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Identity Pathogen/s Overview Distribution Distribution Map for Africa Distribution Table for Africa Hosts/Species Affected Host Animals Systems Affected Epidemiology Impact: Economic Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Prevention and Control References Links to Websites Images
Preferred Scientific Name
malignant catarrhal fever
International Common Names
african malignant catarrhal fever, alcelaphine herpesvirus-1, African MCF, American MCF, bovine malignant catarrh, bovine malignant catarrhal fever, ovine herpesvirus-2, catarrhal fever, European MCF, gangrenous coryza, malignant catarrh, malignant catarrhal fever in pigs, ovine herpesvirus-2, malignant head catarrh, sheep-associated malignant catharral fever, sheep-associated MCF, wildebeest-associated malignant catarrhal fever
alcelaphine herpesvirus 1
alcelaphine herpesvirus 2
caprine herpesvirus 2
ovine herpesvirus 2
Malignant Catarrhal Fever (MCF) is a severe and frequently fatal syndrome of certain clinically susceptible artiodactyl species, caused by one of several herpesviruses to which they are poorly adapted. The causative viruses exist in nature as subclinical infections in other species that serve as carriers; hosts to which they are well adapted.
MCF has a long history in veterinary medicine. The first reports of its recognition as a distinct entity came from France in the late 1700s, and subsequent records of the disease in the literature are scattered throughout the 1800s. The association between wildebeest and MCF in domestic cattle was recognized early on by Maasai pastoralists and by South African farmers, who referred to the disease as snotziekte (snotting sickness) (Plowright, 1965; Metzler, 1991). Experimental studies on MCF began to appear in the first third of the 20th century (Mettam, 1923; Dobberstein, 1925; Götze and Liess, 1929; Daubney and Hudson, 1936). These and other early workers described the basic nature of the disease and began the process of defining the factors governing transmission of the MCF viruses between carrier hosts and clinically susceptible species, a process that continues to this day. A large contribution to the understanding of MCF was made by workers in Africa such Plowright, who isolated the wildebeest (subfamily Alcelaphinae) strain of MCF virus in vitro, and Plowright and Mushi, who conducted numerous experiments to examine the basic epizootiology and pathogenesis of the disease and defined the characteristics of the virus (Plowright, 1964; Plowright, 1990; Mushi and Rurangirwa, 1981a). The characterization of the sheep-associated agent has been constrained by the fact that it has never been successfully isolated, and studies on its biology have necessarily used less direct approaches than were possible with the wildebeest (alcelaphine) strains, which can be propagated in vitro. Development of molecular tools to efficiently detect antibody and viral DNA have in the past decade begun to enable definitive studies on SA-MCF and to facilitate recognition of more subtle disease expressions than classical MCF, including mild and chronic disease (Daubney and Hudson, 1936; Berkman and Barner, 1958; Hamilton, 1990; O'Toole et al., 1995; O'Toole et al., 1997); and recognition of new MCF viruses of neither sheep nor wildebeest origin (Li et al., 2000; Li et al., 2001b).
This description of the clinically relevant aspects of MCF will focus primarily on the two most well characterized viruses, those endemic in wildebeest and domestic sheep. However, it should be noted that many (perhaps most) species of ruminants are endemically infected with viruses that are very closely related to these two agents at a genetic level, and some of these are capable of causing either experimental (Reid and Bridgen, 1991) or natural disease (Li et al., 2000; Li et al., 2001b) in other non-adapted species. Although only a brief mention will be made of these other MCF viruses, future descriptions will of necessity include a number of these emerging members. It is appropriate to refer to these viruses not as 'MCF virus', but rather as 'members of the MCF group' of viruses, whose level of virulence and pattern of disease expression is dependent on both carrier species and the clinically susceptible host.
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
MCF is present anywhere either of the two principal carrier hosts, the domestic sheep or wildebeest, are present. As wildebeest are present in Africa, and elsewhere only in zoos, game farms or zoological gardens, the determining factor for most of the world's MCF is the presence or absence of domestic sheep, which are universally infected with one of the causative viruses. It is likely that MCF is distributed worldwide. Reports exist that document its presence in America, Africa, virtually all the countries of Europe, New Zealand, and many other countries.
For current information on disease incidence, see OIE's WAHID Interface.
= Present, no further details = Widespread = Localised
= Confined and subject to quarantine = Occasional or few reports
= Evidence of pathogen = Last reported... = Presence unconfirmed
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.
|Country||Distribution||Last Reported||Origin||First Reported||Invasive||References||Notes|
|Africa||Present||Plowright et al., 1975|
|Algeria||No information available||OIE Handistatus, 2005|
|Angola||Disease not reported||OIE Handistatus, 2005|
|Benin||No information available||OIE Handistatus, 2005|
|Botswana||Last reported||2002||OIE Handistatus, 2005|
|Burkina Faso||No information available||OIE Handistatus, 2005|
|Burundi||Disease never reported||OIE Handistatus, 2005|
|Cameroon||No information available||OIE Handistatus, 2005|
|Cape Verde||Disease never reported||OIE Handistatus, 2005|
|Central African Republic||Disease not reported||OIE Handistatus, 2005|
|Chad||No information available||OIE Handistatus, 2005|
|Congo Democratic Republic||No information available||OIE Handistatus, 2005|
|Côte d'Ivoire||Disease not reported||OIE Handistatus, 2005|
|Djibouti||Disease not reported||OIE Handistatus, 2005|
|Egypt||No information available||OIE Handistatus, 2005|
|Eritrea||Reported present or known to be present||OIE Handistatus, 2005|
|Ghana||Disease not reported||OIE Handistatus, 2005|
|Guinea||Disease never reported||OIE Handistatus, 2005|
|Guinea-Bissau||No information available||OIE Handistatus, 2005|
|Kenya||CAB Abstracts data mining||Kalunda et al., 1981; OIE Handistatus, 2005|
|Libya||Disease never reported||OIE Handistatus, 2005|
|Madagascar||Disease never reported||OIE Handistatus, 2005|
|Malawi||No information available||OIE Handistatus, 2005|
|Mali||No information available||OIE Handistatus, 2005|
|Mauritius||Disease not reported||OIE Handistatus, 2005|
|Morocco||Reported present or known to be present||OIE Handistatus, 2005|
|Mozambique||No information available||OIE Handistatus, 2005|
|Namibia||Reported present or known to be present||OIE Handistatus, 2005|
|Nigeria||No information available||OIE Handistatus, 2005|
|Réunion||No information available||OIE Handistatus, 2005|
|Rwanda||No information available||OIE Handistatus, 2005|
|Sao Tome and Principe||No information available||OIE Handistatus, 2005|
|Senegal||No information available||OIE Handistatus, 2005|
|Seychelles||Disease not reported||OIE Handistatus, 2005|
|Somalia||No information available||OIE Handistatus, 2005|
|South Africa||Reported present or known to be present||Metzler, 1991; Barnard, 1990; Mettam & Snotsiekte, 1923; Plowright, 1965; Barnard & van, 1988; OIE Handistatus, 2005|
|Southern Africa||Widespread||Barnard et al., 1994|
|Sudan||Disease not reported||OIE Handistatus, 2005|
|Swaziland||Disease not reported||OIE Handistatus, 2005|
|Tanzania||No information available||OIE Handistatus, 2005|
|Togo||Disease never reported||OIE Handistatus, 2005|
|Tunisia||Last reported||2000||OIE Handistatus, 2005|
|Uganda||Disease not reported||OIE Handistatus, 2005|
|Zambia||No information available||OIE Handistatus, 2005|
|Zimbabwe||Reported present or known to be present||OIE Handistatus, 2005|
The natural hosts for the MCF viruses are found within the artiodactyl families the Bovidae, Cervidae, and Giraffidae. Two types of hosts exist: well-adapted asymptomatic carriers, and poorly adapted hosts, in which both clinical disease and latent subclinical infections occur. The well-adapted carrier hosts shed virus into the environment and are capable of transmitting it to clinically susceptible hosts when contact is sufficiently close, or when indirect means of transfer of virus, such as suitable fomites, are present. Poorly adapted hosts are generally considered not to shed infectious virus, and therefore to be dead-end hosts. The families Cervidae and Giraffidae have to date been found to contain only clinically susceptible species. The family Bovidae contains both carrier and clinically susceptible species. The Bovinae tend to contain clinically susceptible species, whereas members of other subfamilies, such as Caprinae, Alcelaphinae, and Hippotraginae, are generally well-adapted carriers. However exceptions exist, and a full picture of the various viruses involved in the MCF syndrome, and the relative susceptibility of the various mammalian taxa to those viruses cannot be constructed until more data is available.
Two principal viruses are responsible for most MCF seen in domestic animals. One exists as a ubiquitous infection in various species of wildebeest (subfamily Alcelaphinae), and is known as alcelaphine herpesvirus-1 (AlHV-1). It is present on the African continent and in zoos and game farms anywhere in the world that these species are kept. The other major MCF virus exists as a ubiquitous infection in domestic sheep (Ovis aries), and is referred to as the sheep-associated MCF virus, or ovine herpesvirus-2 (OvHV-2). Because of the cosmopolitan distribution of sheep, OvHV-2 is responsible for most cases of MCF worldwide. MCF of OvHV-2 origin and AlHV-1 origin cannot be distinguished from one another clinically or histopathologically. Domestic goats harbor their own closely related strain of MCF virus, which has been termed caprine herpesvirus-2 (CpHV-2) (Li et al., 2001b). Disease caused by this virus has to date been described only in deer so its pathogenicity is not yet well defined.
It is becoming increasingly clear that many other ruminant species harbor their own strains of well-adapted rhadinoviruses that are very closely related to the ovine and wildebeest viruses. Rather than simply using the term 'MCF virus', it is probably more appropriate to refer to these agents as an 'MCF-group virus', as MCF can be caused by any one of several members of a closely related group. Some of the viruses appear to cause spontaneous disease in other species (Li et al., 2001b), and others do not (Mushi et al., 1981a; Castro and Heuschele, 1985). Moreover, MCF-group viruses have been found in deer in the terminal stages of MCF, the species of origin for which it has not yet been identified (Li et al., 2000). The known number of ruminant species harboring members of this group will undoubtedly expand as research progresses.
MCF can occur in domestic pigs, producing an acute and lethal disease with typical lesions. A number of reports of an MCF-like disease in swine on farms where sheep were also present have appeared from Europe over the last two decades or so; the disease was recently confirmed to be due to OvHV-2 infection (Loken et al., 1998). Little is yet known about epidemiology or pathogenesis in pigs.
The domestic rabbit (Oryctolagus cuniculus) is readily infected experimentally with both wildebeest and ovine MCF viruses, and develops significant lymphoproliferative disease that may have promise as a comparative disease model (Plowright, 1964; Plowright, 1990). Other laboratory animals that have been successfully infected include the rat and hamster (Reid et al., 1986).
|Bison bison||Wild host|
|Bos indicus (zebu)||Domesticated host|
|Bos javanicus||Domesticated host|
|Bos taurus (cattle)||Domesticated host|
|Bubalus bubalis (buffalo)||Domesticated host|
|Cervus dama||Domesticated host, Wild host|
|Cervus elaphus (red deer)||Domesticated host, Wild host|
|Odocoileus hemionus||Wild host|
|Odocoileus virginianus||Wild host|
|Sus scrofa (pigs)||Domesticated host|
Blood and Circulatory System - Large Ruminants
Blood and Circulatory System - Pigs
Blood and Circulatory System - Small Ruminants
Digestive - Large Ruminants
Digestive - Pigs
Digestive - Small Ruminants
Multisystem - Large Ruminants
Multisystem - Pigs
Multisystem - Small Ruminants
Nervous - Large Ruminants
Nervous - Pigs
Nervous - Small Ruminants
Respiratory - Large Ruminants
Respiratory - Pigs
Respiratory - Small Ruminants
Skin - Large Ruminants
Skin - Pigs
Skin - Small Ruminants
MCF is predominantly a disease of domestic cattle (Bos taurus and B. indicus), water buffalo (Bubalus bubalis), Bali cattle (banteng; Bos javanicus), American bison (Bison bison) and deer (cervid species). However, extensive lists of clinically-susceptible species of ruminants, primarily belonging to the subfamilies Bovinae, Cervinae, and Odocoileinae have been compiled from cases occurring in zoos and on game farms (Plowright, 1981; Heuschele, 1988). Both of the two major strains of MCF virus, the ovine and wildebeest strains, are capable of causing indistinguishable disease in any of these species. The general factors affecting animal-to-animal transmission such as viral stability, environmental factors, and spatial considerations are those that might be expected for a herpesvirus: efficient transmission via infected secretions is favored by close contact and a cool, moist environment. The virus is relatively unstable in the environment, losing over 99.9% of its titre within 3 hours under hot, dry weather conditions (Rossiter et al., 1983). The epidemiology of the two major MCF viruses, the alcelaphine and the ovine viruses, within their natural, well-adapted hosts differs significantly, and so they are discussed separately.
The epidemiology of clinical MCF, that is patterns of virus transmission from well-adapted host to non-adapted or 'susceptible' host, is better defined for the alcelaphine virus than for the other strains. In contrast to the ovine virus, the alcelaphine virus can be propagated in vitro, it more readily induces experimental disease, and can be isolated and titrated from tissues and secretions of clinically-susceptible hosts; thus it has been more thoroughly characterized. Both viruses are shed into the environment via oral, nasal, and possibly ocular secretions from their respective well-adapted reservoir hosts in a manner similar to rhadinovirus infections of primates and humans. Clinically susceptible species acquire the virus through inhalation, ingestion of virus-laden secretions, or through ingestion of contaminated foodstuffs or water.
The wildebeest-associated MCF (WA-MCF) virus (WA-MCFV) is harbored by all species of wildebeest as a lifelong, asymptotic infection. Viral shedding by adults is at relatively low levels, except during periods of stress or parturition, at which time infectious virus titres in oropharyngeal and ocular secretions rise significantly (Plowright, 1986). Although MCF is occasionally transmitted from adult wildebeest, most clinical disease originates from young wildebeest calves up to the age of about 4 months. Epidemiology within wildebeest species involves both horizontal and vertical transmission. Occasionally wildebeest calves are born infected through the transplacental route. Most calves, however, are infected horizontally from previously infected cohorts, which develop viremia and shed virus through ocular and nasal secretions (Mushi et al., 1981b; Plowright, 1990). Infectivity titres in wildebeest calf secretions exceed 103 TCID50 /ml during peak shedding periods, most of which is cell-free (Mushi et al., 1980). Neutralizing antibody develops by about 3 months of age, after which viral shedding declines dramatically (Mushi et al., 1981b).
Whereas WA-MCF occurs most frequently in Africa during the wildebeest calving season, in zoological parks sporadic cases occur throughout the year. Most shedding from adult wildebeest is in the form of highly cell-associated virus, but cell-free virus shedding can be induced by stress (Plowright, 1986) or steroid administration (Rweyemamu et al., 1974). WA-MCFV is not transmitted by natural means from one clinically susceptible host to another; affected animals are dead-end hosts. As opposed to the ovine strain, WA-MCFV can be readily transmitted experimentally among clinically-susceptible species by injection of blood or tissue, but little or no cell-free virus is shed into secretions (Mushi and Rurangirwa, 1981b), therefore these animals generally pose no hazard for their herd-mates. However, the virus occasionally passes via intrauterine transmission from latently infected domestic cows to their calves (Plowright et al., 1972; Barnard, 1990).
Experimental transmission of the sheep-associated MCF virus (SA-MCFV) from a clinically affected cow to another cow is much more difficult than that for the wildebeest strain of virus. On the few reported occasions where transmission has been successfully accomplished, it has required the transfer of large volumes of very fresh blood or tissue suspension (Selman et al., 1978; Pierson et al., 1974). This suggests that infectivity titres in diseased animals are lower in animals infected with the ovine strain of virus than with the wildebeest strain. Field observations of many natural outbreaks and substantial experimental data indicate that horizontal transmission from clinically ill cattle does not normally occur (Farquharson, 1946; Mare, 1977). Transmission of the ovine strain between members of clinically susceptible species may be somewhat more easily accomplished in some highly clinically susceptible species of deer, such as Père David's (Huck et al., 1961).
The epidemiology of ovine MCF virus within sheep is somewhat controversial. Baxter et al. (1997) reported that all the lambs in their experimental study were infected by 2 months of age, similar to wildebeest calves. However, there are contraindications from other studies that transmission of the sheep virus differs from the wildebeest strain in some significant aspects. Whereas intense viral shedding from the wildebeest occurs predominantly during the first 90 days of life, lambs do not begin to shed significantly until after 5 months of age (Li et al., 1998). Although occasional intra-uterine infections occur in sheep, the majority of lambs are not infected until after 2-2.5 months of age under natural flock conditions. If removed from contact with infected sheep prior to that age, lambs remain uninfected and can be raised free of the virus (Li et al., 1999). This method is being used by sheep producers and zoos in the USA and in Europe to produce virus-free sheep (Muller-Doblies et al., 2001). This would seem to support the concept of delayed, rather than congenital or perinatal infection of lambs.
Transmission of clinical SA-MCF occurs both from adolescent lambs and from adults. Viral DNA levels form a distinct peak in oronasal secretions in the 6 to 8-month age range, and then decline to lower levels, which persist with only limited fluctuations for the life of the sheep. However there are often significant differences in levels of shedding between adult sheep. No correlation between parturition and shedding levels has been found, suggesting that the likelihood of transmission from a given adult sheep is relatively stable all year-round. Moreover, the much higher levels in the secretions of adolescent lambs (Li et al., 2001a) suggests a higher likelihood of transmission from them than from adults given equal exposure conditions. In contrast to bovine WA-MCF, bovine SA-MCF occurs year-round (Farquharson, 1946; Barnard et al., 1994), with only a moderately higher incidence during the lambing season (Harris et al., 1978; Muller-Doblies et al., 2001). The moderate increase at this time could reflect factors other than shedding levels, such as climatic conditions and seasonal variations in stocking densities that could influence exposure intensity. In American bison (Bison bison), MCF is a late-autumn and winter disease, with no discernable peak around the time of lambing. It is likely that the distinct seasonality associated with the wildebeest strains has historically exerted an unwarranted influence on judgments concerning the seasonality of sheep-associated MCF.
The main source of WA-MCF virus for transmission has clearly been shown to be nasal and ocular secretions (Mushi et al., 1980; Plowright, 1990). In sheep, the very high levels of viral DNA in nasal secretions relative to the blood suggests that this is also the normal mode of transmission of the ovine virus (Li et al., 2001a). However, successful experimental transmission of the disease by transfer of secretions has not been reported. Field observations indicate that the virus is transmitted most efficiently by intimate contact, but that remote transmission, presumably by shared water sources and other ill-defined routes is possible. For example, natural transmission to highly susceptible species of deer and to bison at distances of up to several hundred meters has been reported.
A significant feature of the epidemiology of MCF is the often-perplexing phenomenon of clinical cases occurring in the absence of any obvious carriers such as sheep or wildebeest. Much discussion and confusion has arisen around this issue, stimulating the postulation of a variety of alternate transmission modes ranging from insect vectors to horizontal transmission between susceptible animals (Piercy, 1954b; Huck et al., 1961; Erasmus, 1986; Barnard and van de Pypekamp, 1988; Schultheiss et al., 2000). For a review of contributions of early workers to this subject see Plowright (1964). Significant prevalence rates of antibody against the MCF group of viruses has been repeatedly shown in many clinically susceptible ruminant species, using a variety of lab tests (Rossiter and Pandey, 1985; Reid and Buxton, 1989; Metzler, 1991; Barnard et al., 1994). Recorded seropositivity rates indicate that a large pool of latent infection by these herpesviruses exists among populations of clinically susceptible species. That recrudescence of latent MCFV infections is a common phenomenon, as in many other herpesviruses, has been shown and discussed by a number of researchers (Piercy, 1954a; Reid and Buxton, 1989); however, only lately has its level of significance begun to be appreciated. Recrudescence will probably be shown to explain much of the enigmatic epidemiology commonly associated with MCF.
The economic loss caused by MCF has not been quantified. In cattle, in particular the European breeds, it is generally a sporadic, low-morbidity disease, with isolated cases occurring at unpredictable intervals. Occasionally however, MCF outbreaks reach severe proportions, resulting in death of many cattle over a period of a few weeks or months (Farquharson, 1946; Pierson et al., 1973; Mare, 1977; Orsborn et al., 1977; Hamdy et al., 1978; Collery and Foley, 1996). In Africa, MCF is responsible for very significant losses in domestic cattle herds, estimated in 1970 to be about 7% annually (Plowright et al., 1975). MCF is frequently devastating to operations involving highly susceptible species, such as bison, banteng, and many species of deer. It is emerging as a serious problem for bison breeding and feeding operations in the USA, where MCF-caused losses in feedlots can approach 10% of animals (Schultheiss et al., 2000; O'Toole et al., 2002). Small-scale bison raisers have been put out of business by MCF subsequent to the movement of infected sheep onto neighbouring farms.
Persistent sporadic to near-epidemic-level losses from MCF are common among operations which allow susceptible species to come in contact with sheep, and to a lesser extent, domestic goats. This applies to deer farms, exotic game farms, research herds and zoological collections the world over. One report showed that over 40% of the annual death losses in farmed deer were likely to have been caused by MCF (Beatson et al., 1985). The disease has destroyed entire collections of rare deer species (Castro and Heuschele, 1985). Moreover, until recent years, the imprecision of diagnostic tests for clinical MCF resulted in significant numbers of misdiagnoses, particularly in mild or atypical cases. Therefore the true incidence is higher than commonly believed, due to widespread under-diagnosis (Selman, 1987; O'Toole et al., 1997).
The MCF group of gammaherpesviruses appears to be well adapted to the artiodactyls, and do not normally infect other mammals or birds. They are not known to present any zoonotic hazard.
Gross lesions are quite variable, depending on the species affected, and both severity and duration of clinical illness. The nasal and oral mucus membranes are inflamed, with either focal or diffuse necrosis, erosion and ulceration. Erosions may be found anywhere along the alimentary tract, from the muzzle to the colon. Punctate or larger ulcers are common on the gums, palate, tips of the oral papillae, oesophagus, abomasum, rumen, and both small and large intestine. Erosions in the oesophagus and intestine may be linearly oriented. Ulcerated areas, often covered by fibrin, are frequent in the mucosa of the nose and turbinates, as well as in the gastrointestinal tract. Significant gross lesions are not common in the lungs per se, other than occasional non-specific interstitial emphysema. Ocular panophthalmitis underlies conjunctivitis and corneal oedema. Lymph nodes may be grossly swollen, particularly in cattle. Fibrin may be found in inflamed joints of lame animals. Bladder lesions are common, consisting of focal areas of haemorrhage and swelling. More chronic presentation of MCF can result in prominent renal arteries that are accentuated by scarring, comprised of intimal, medial and perivascular fibroproliferation. This lesion is most common in cattle, but is also seen in deer, water buffalo and occasionally in other species. Other organs such as the heart, brain and liver generally do not exhibit significant gross abnormalities.
Microscopically, infiltrations of proliferating lymphocytes and other mononuclear cells are found in most organs, with particular orientation to vascular structures and beneath inflamed mucous membranes. The classic histologic lesion is inflammation and fibrinoid necrosis of the media of small muscular arteries, but these lesions may be difficult to locate, particularly in the more rapidly fatal cases. No inclusion bodies are seen in the disease. Likewise, all reported attempts to demonstrate viral antigens in tissues have been unsuccessful. Diagnosticians should be aware that significant differences exist between clinically susceptible species in the organ-specific character and severity of MCF lesions (Schultheiss et al., 2000; O'Toole et al., 2002). Detailed species-specific descriptions are beyond the scope of this data sheet. Where appropriate, diagnosticians should consult pathology references for specifics (Berkman and Barner, 1958; Huck et al., 1961; Clark et al., 1970; Wyand et al., 1971; Selman et al., 1974; Hatkin, 1980; Liggitt and DeMartini, 1980a,b; Zimmer et al., 1981; Whiteley et al., 1985; Plowright, 1990; O'Toole et al., 1995).
Strong suspicion of MCF should be raised if animals of a clinically susceptible species present with characteristic signs at a low morbidity rate. A history of contact with sheep, goats or wildebeest is also indicative, although this contact is often non-apparent or absent in many cases that occur as a result of recrudescence. Swollen nodes, corneal oedema, erosive and inflammatory changes in the gastrointestinal tract, and skin and bladder lesions are all compatible with the diagnosis. Pathologists consider that vascular lesions if present are highly indicative of MCF. Animals suspected of MCF should be necropsied promptly after death, because autolysis is often significant in large animals. Tissues (lymph node, spleen, lung, brain, gut, thyroid, adrenal, affected skin, etc) should be submitted for histological examination fixed in formalin. Fresh tissues should be promptly refrigerated and submitted unfrozen for virus isolation. Virus isolation may assist in the differential diagnoses with mucosal disease and IBR, or be a prerequisite for the isolation of the wildebeest strain, or to provide a source of DNA for the definitive lab test for acute MCF: demonstration of viral DNA by PCR (Katz et al., 1991; Baxter et al., 1993; Li et al., 2001b).
Polymerase chain reaction (PCR)
EDTA-anticoagulated blood should be submitted from live animals for PCR on peripheral blood leukocyte DNA. Any animals that are suffering from MCF will have sufficient levels of viral DNA in their leukocytes and tissues to be readily detected by PCR. If fresh blood or tissue is not available, PCR (Tham, 1997; Crawford et al., 1999) and in situ hybridization (Michel et al., 1997) can be effectively run on DNA extracted from fixed and embedded tissues, assuming fixation time did not exceed 3-4 weeks. For longer-term storage, tissues can be preserved for PCR in 70-80% ethanol (Crawford et al., 1999). Careful PCR primer selection by the laboratory is important, because PCR tests are generally specific for a given strain of virus. For example, primers currently in widespread use for the sheep agent (OvHV-2) (Baxter et al., 1993) will not detect DNA of the wildebeest agent (AlHV-1), nor of the more recently-described goat virus (CpHV-2). Until broader-spectrum primers for specific detection of the entire MCF-group of viruses are developed, the clinician should inform the laboratory as to which MCF agent is suspected in order to guide the lab in selection of appropriate primers.
A broad array of serological assays has been used to detect antibody against MCF viral antigens; these are generally conducted in only a few laboratories in each country. Most diagnostic labs will forward samples to appropriate labs that are capable of MCF testing. Serologic tests that have been used include viral neutralization, complement fixation, indirect immunofluorescence or immunohistochemistry, direct-binding ELISA, and competitive-inhibition ELISA (CI-ELISA). Viral neutralization tests utilize the alcelaphine virus for a neutralization target, and are reliably specific for the MCF group of viruses. Neutralizing antibody against the sheep agent cross-reacts with the alcelaphine virus, albeit weakly, so it has been used to detect antibody against OvHV-2 as well as AlHV-1. Polyclonal assays other than viral neutralization can suffer from non-specificity arising from well-documented sharing of antigens between different herpesviruses (Heuschele, 1988; Metzler, 1991). These tests require very careful interpretation on the part of the operator. The viral neutralization test, though a highly specific assay for anti-MCF antibody, is labour-intensive and expensive, and works better for antibody against the alcelaphine than the ovine or caprine viruses. The CI-ELISA, a monoclonal-based assay that is specific for the antibody against the MCF group of viruses is rapid and economical. Reagents for this assay are commercially available, and the number of labs offering the test are increasing (Li et. al., 2001c).
Serological results must be interpreted with certain features of MCF in mind. Animals that die quickly may not develop detectable levels of antibody prior to death. Also, the significant percentages of cattle, bison and other clinically susceptible species that are latently infected provide a sizeable pool of clinically normal yet seropositive animals. The presence of antibody alone is not etiologically diagnostic. Rather diagnosis requires demonstration of significant levels of viral DNA in the blood or tissues by PCR. The main usefulness of serology is for the surveying of subclinically infected individuals in a herd.
The transmission of one of the virulent strains of MCF viruses from their carrier hosts to clinically-susceptible ruminants can initiate the syndrome of classic malignant catarrhal fever, which is an acute polysystemic disease characterized by lymphoproliferation and inflammation oriented toward mucosal surfaces and blood vessels. Reported incubation periods vary widely, and are of limited usefulness in MCF, as there are numerous complicating factors that affect disease expression. Recrudescence of existing infections for example, can occur at any time, giving the impression of extremely prolonged incubation periods. Estimates from studies of experimental exposures have ranged from 9 to over 60 days (Plowright et al., 1960; Huck et al., 1961; Plowright, 1968). Reported incubation periods of several months or more probably represent recrudescences of previously established infections.
Classical MCF cases are often but not always fatal. The case-fatality rate varies with the species of animal and perhaps with the particular virus involved. Highly susceptible species such as bison, banteng, and some cervid species generally experience shorter, more acute courses than do less susceptible species such as domestic cattle. It is a common observation that those animals that die the fastest are often the ones in 'best flesh' (Farquharson, 1946). Many deer die within 48 hours of the first signs of MCF, but this timeframe is highly variable; some linger for weeks before dying, and a few recover. Bison generally expire within 4-7 days of initial signs; only occasional affected animals experience subacute or chronic manifestations. A higher percentage of affected cattle than deer or bison will survive longer than a week. It has been suggested that strains of varying virulence exist, some more prone to producing mild disease and recovery than other strains (Daubney and Hudson, 1936). Mild cases which recover have been observed more frequently in cattle than in other species (Hamilton, 1990). Studies indicate that as many as one-third of cattle with clinical MCF exhibit chronic symptoms, surviving for several weeks to months (Berkman and Barner, 1958; O'Toole et al., 1997) and developing characteristic chronic MCF lesions (O'Toole et al., 1995). A few eventually recover completely, but most either recrudesce suddenly and die, or linger indefinitely as 'poor-doers'.
Disease generally presents suddenly, with little preliminary indications of illness. Although there are some rather constant signs, there is also considerable variability in presentation. Typical signs in cattle include sudden fever, drop in milk production, inappetance, and serous discharge from the eyes and nose with matting of facial hair. Temperature may spike to 106°F for a day or two before declining to 103-104°F. Within a day or two of initial signs, corneal edema appears, typically starting around the limbus and spreading centrally. Episcleral injection, lid swelling and sensitivity to light are common. Deep corneal inflammation frequently progresses to blindness within 4-5 days. Prolonged inflammation of the cornea can terminate in perforation and herniation of the iris. Nasal exudate becomes mucoid in character within a few days, with mucopurulent discharges from the nose, stertorous breathing, and often dyspnea. The muzzle epithelium is initially inflamed and later necrotic, resulting in encrustation, cracking and often dislodging of affected epithelial patches to reveal the underlying inflamed subepithelium. At this stage, animals are usually severely depressed, and may separate from herd mates and stand immobile with head hanging. CNS involvement is common, however, and can lead to hyperexcitability, aggressiveness, twitching, incoordination, nystagmus, and muscular tremors.
Skin lesions are common in cattle and deer with infection with ovine MCFV, and with the recently described caprine virus, but less so with the wildebeest virus (Plowright, 1990). Areas of erythema and exudation may be found in any area of the body, including the bulbs of the heels and between the digits. Affected skin often becomes thickened and corrugated in appearance. Either generalized or patchy hair loss is prominent, tending to predominate over the cervical region, along the spino-dorsal axis, or on the medial aspects of the hind limbs. Small, elevated circumscribed areas may be present on the udder or vulva. The skin of the teats and udder may become inflamed, then dry, thicken and crack, leading to fissure formation and scabbing.
The widespread inflammatory process can include the joints. Signs of arthritis may be seen, including joint puffiness, shifting of weight and reluctance to move. Generalized lymph node swelling is the rule in cattle, and can often be seen in the prescapular or inguinal nodes. This feature is either not as prominent or not as easily detected in bison. Diarrhoea is uncommon in cattle, but more frequent in bison and deer, in which it is often bloody. Urine may be bloody, as haemorrhagic cystitis is common.
Götze (1930) divided the clinical presentation of MCF into 4 'forms':
- head and eye
Berkman and Barner (1958) proposed addition of a fifth category of 'chronic'. However there is little underlying data on differences in pathogenesis that support this categorization. Although there is some diagnostic usefulness to the scheme, it should be borne in mind that rather than being distinct and clearly delineated, there is much overlap between the 'forms' and therefore the classification may be of only limited value (Heuschele, 1988).
No practical, consistently effective treatments are available. Many therapeutic attempts have been described, including the use corticosteroids, antibiotics, antivirals, vitamins, and other supportive treatments. Occasional reports exist of recovery of cattle following treatment, typically with corticosteroids (Milne and Reid, 1990; Penny, 1998), but the role of the treatment remains to be proven, as significant numbers of cattle also recover without treatment (Kalunda et al., 1981; Hamilton, 1990; O'Toole et al., 1997).
The prevention of contact between carriers and clinically susceptible species remains the primary method of disease control. Scrupulous care should be taken to avoid contact between sheep, wildebeest, and goats; and deer, bison, Bali cattle, water buffalo, and to a lesser extent, European breeds of cattle. Operations that depend upon mixing species, such as petting zoos, may wish to consider producing their own virus-free sheep or goats (Li et. al., 1999). Reduction of stress is also beneficial in reducing the number of cases, particularly in the more susceptible species. No vaccine is available.
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Date of report: 03/06/2013
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