Preferred Scientific Name
International Common Names
- English: BPV infection; buffalo pox
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In India, outbreaks of pox disease amongst domestic buffaloes (Bubalus bubalis) have been recognised since 1934 (Sharma, 1934). Early reports considered it to be related to infection with variola or vaccinia viruses; the term buffalopox was not used until Haddow and Idnani (1949). Buffalo calves had been used extensively for production of vaccinia virus for vaccination of humans against smallpox and some had suspected that this was the origin of the outbreaks. However, the persistence of outbreaks after the cessation of human vaccination suggested that the disease could persist independently. DNA analysis has suggested that buffalo poxvirus may be conspecific with vaccinia (Dumbell and Richardson, 1993).
The disease has now been described from a number of other countries where buffalo are important domestic animals, including Pakistan, Bangladesh, Indonesia and Egypt (Lal and Singh, 1977). In addition to buffalo, cattle have been reported to have become infected in some outbreaks (Ghosh et al., 1977; Sehgal et al., 1977; Yadav et al., 2010; Tarang Goyal et al., 2013). Cases of zoonotic human infections with buffalo poxvirus, mostly among animal attendants, milkers and laboratory workers have been reported regularly since the first report in buffalo (Kolhapure et al., 1997; Bhanuprakash et al., 2010; Tarang Goyal et al., 2013; Thachamvally Riyesh et al., 2014).
Clinically the disease is typical of a non-fatal poxvirus infection with characteristic pocks developing over the skin of the udder and teats of milking animals and the heads of suckling calves; lesions are described to have become generalised in some animals (Katana, 1969; Bhanuprakash et al., 2010). The course of infection generally runs for 4-8 weeks and recovered animals have brown scars where lesions have resolved. The main economic impact is due to reduced milk production, which can become complete and result in mastitis through stenosis of the milk canal.
Infection in humans is usually restricted to one to five lesions affecting the hands and forearms. Human-to-human infection was formerly not considered to occur. However, this view has been challenged as outbreaks in humans have occurred with a longer duration and more severe symptoms in individuals that have had no confirmed contact with buffaloes (Kolhapure et al., 1997). Nosocomial spread between hospital burns units in Karachi, Pakistan, was reported by Afia Zafar et al. (2007).
Since 2006, mass outbreaks of buffalopox in domestic buffaloes, along with severe zoonotic infection in milk attendants, have been reported in several regions in India (Bhanuprakash et al., 2010; Venkatesan et al., 2010). In some outbreaks, infections were also recorded in cows in the same herds (Yadav et al., 2010). An increase in buffalo poxvirus transmission to different species, including buffaloes, cows, and humans, suggests the reemergence of zoonotic buffalopox infection (Bhanuprakash et al., 2010; Bera et al., 2012). Shchelkunov (2013) speculates that since outbreaks have been recorded in different distant regions of India, there is likely to be an abundant natural buffalo poxvirus reservoir represented by wild animals, possibly rodents.
Most outbreaks of disease affect only buffaloes and humans although some also involve cattle (Ghosh et al., 1977).
Infection is most frequently recognised in milking animals with lesions appearing on the teats and udders, whereas in humans lesions are mainly on the hands and forearms of milkers, where they have come into contact with infected animals.
Infectivity experiments revealed buffalo poxvirus is transmissible to buffaloes, cows, rabbits, guinea-pigs and suckling mice, whereas sheep, goats, fowl and adult mice were found refractory to infection (Singh et al., 1996).
Buffalopox is endemic in India and has been reported from many other areas where buffaloes are farmed for milk or draught, including Pakistan, Bangladesh, Indonesia and Egypt (Lal and Singh, 1977).
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 details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Russia||Present||Present based on regional distribution.|
Rana et al. (1988) intradermally infected 6-month-old buffalo calves with buffalo poxvirus; infected and control animals were killed over 17 days. Primary lesions of erythema and papules followed on days 2-3, then vesicle and pustule formation on days 4-5 and scab formation on day 10; ulcers had healed by 28 days. Pyrexia was apparent from days 2-9 and lacrimation and nasal discharge between days 5-9. Four buffalo calves developed diarrhoea. Secondary skin lesions appeared between days 6-8. Regional lymph nodes were enlarged and congested from days 2-6. The lungs were congested and emphysematous from days 5-9. Hepatic and splenic focal necrosis appeared from days 5 and 6. The abomasal serosa developed nodules between days 6-10. The intestine had haemorrhages and enlarged Peyer's patches.
Chandra et al. (1986) reported that experimental infection of rabbits produced typical skin lesions at the site of primary inoculation, following an incubation period of 48-72 h. Gross lesions in internal organs, characterized by focal or diffuse necrotic areas on the lungs, liver and spleen were seen from day 5 after inoculation. Isolated lesions of approximately 2 mm diameter appeared in the skin, stomach, intestine and uterus from day 7. Histopathological changes, including intra-alveolar and intra-bronchial haemorrhages, were seen in lungs and severe fatty changes were found in the liver. Multinuclear cells were detected in the liver during recovery.
Diagnosis is often made on clinical grounds alone. Virus in scabs can be detected by electron microscopy and may be cultivated in embryonated eggs or tissue culture cells such as RK-13, chick embryo fibroblasts, BHK21 or Vero cell lines (Baxby and Hill, 1971; Manoharan et al., 2009). Various serological assays have been developed for diagnosis of buffalopox, including agar gel immunodiffusion test (AGID), counter-immunoelectrophoresis (CIE), serum neutralization test (SNT), ELISA and immunoperoxidase test (IPT); however, these tests may fail to accurately diagnose the disease due to antigenic cross-reactivity (Singh et al., 2007). A specific and sensitive PCR assay for the diagnosis of buffalopox is described by Singh et al. (2008).
|Reproductive Signs / Agalactia, decreased, absent milk production||Cattle & Buffaloes|Cow||Diagnosis|
|Reproductive Signs / Firm mammary gland, hard udder||Cattle & Buffaloes|Cow; Cattle & Buffaloes|Heifer||Sign|
|Reproductive Signs / Obstruction of milk outflow||Cattle & Buffaloes|Cow||Sign|
|Reproductive Signs / Teat injury, cut, tear||Cattle & Buffaloes|Cow; Cattle & Buffaloes|Heifer||Sign|
|Reproductive Signs / Vulval ulcers, vesicles, erosions, tears, cuts, pustules, papules||Cattle & Buffaloes|Cow; Cattle & Buffaloes|Heifer||Sign|
|Skin / Integumentary Signs / Scarred skin||Cattle & Buffaloes|All Stages||Sign|
|Skin / Integumentary Signs / Skin crusts, scabs||Cattle & Buffaloes|All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin papules||Cattle & Buffaloes|All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin pustules||Cattle & Buffaloes|All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Cattle & Buffaloes|All Stages||Sign|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Cattle & Buffaloes|All Stages||Diagnosis|
|Skin / Integumentary Signs / Warm skin, hot, heat||Cattle & Buffaloes|All Stages||Sign|
Both generalised and localised forms of the disease have been described in affected buffaloes whereas humans may experience a systemic reaction. In buffalo, the disease is characterised by the development of typical poxvirus lesions mainly on the teats, udder, inner thigh and in some cases around the lips, nostrils, ears and eyes. In some cases pocks are distributed extensively over the body. Typical lesions progress from papule to vesicle to pustule to scab, which is in turn replaced by an ulcer in 10-15 days that leaves a brown scar when resolved. In all milking animals yields are reduced and in some cases stenosis of the milk canal may occur, resulting in mastitis and cessation of milk production. Full recovery may take 1-2 months.
In humans, lesions are seldom more than five in number and are usually restricted to the hands and forearms. Infection is associated with fever lasting up to 5 days which commences shortly after lesions are first observed. Lesions will normally resolve after 2 weeks, leaving superficial scars.
Reports suggest that buffalopox outbreaks in India are becoming more severe. Four outbreaks of buffalopox in domestic buffaloes, with high case fatality rates in young buffalo calves, high morbidity with significant productivity loss in adult animals, and severe zoonotic infection in milk attendants were recorded at various places in India, during 2006-2008 (Bhanuprakash et al., 2010). In buffaloes, the pox lesions were confined to udder and teats of the majority of the affected animals; in a few animals the lesions appeared on the hindquarters, indicating generalized infection. The overall disease morbidity, mortality and case fatality rate were 6.8%, 0.7% and 11.4%, respectively. Milkers developed pox-like lesions on the hands, forearms and forehead accompanied by fever, axillary lymphadenopathy and general malaise.
A severe outbreak involving many human cases was recorded in Kolhapur (Maharashtra), India in 2009 (Venkatesan et al., 2010). The outbreak involved 4000 buffalo from 21 villages and 125 humans, who were mostly animal handlers and milkers of all age groups. Pox lesions were observed on all parts of the body of the animals; the most severe were on the inner ear, which led to otitis and pyrexia. Milkers developed pox-like lesions on the skin of their fingers, hands, forearms, forehead, ears and face, along with pyrexia, malaise and axillary lymphadenitis and lymphadenopathy.
Tarang Goyal et al. (2013) reported a buffalopox outbreak with atypical features in Uttar Pradesh, India. Lesions were present on the eyes, hands, fingers, legs and feet of patients. Two patients developed severe lesions on the left eyelid that progressed from the vesicular stage leading to the development of severe inflammation and corneal opacity within 7-10 days. Lesions were present in the children of milkers, suggesting spread by fomites.
Disease is regularly reported from buffalo-rearing areas in India. The disease has mainly been recorded in young and old buffaloes during the epidemics (Singh et al., 2007), but cattle are occasionally affected (Ghosh et al., 1977). Humans, particularly milkers, contract infection upon close contact with infected animals (Singh et al., 2007). The spread of infection among animals and humans in villages is probably facilitated by direct contact between affected and healthy animals, between dairy personnel and also by animal trade between villages (Singh et al., 2006; Venkatesan et al., 2010).
An overall disease prevalence rate of 10.13% was reported in one study of buffalopox, in which there was no significant difference between prevalence in adult male (13.63%) and adult female (13%) and young male (6.32%) and young female buffaloes (5.24%) (Kumar et al., 1987). A higher prevalence (23.4-79.4%) was reported in outbreaks in Karnataka (Muraleedharan et al., 1989). The spread of disease in these outbreaks was rapid and biting flies such as Lyperosia exigua [Haematobia irritans exigua], Musca crassirostris and M. vicina [M. domestica vicina] aggravated the sores. The authors suggest that flies may be involved in mechanical transmission.
Buffalopox is an economically significant disease in states of India where buffalo are important, with losses occurring through lost milk production and development of mastitis, decreased meat yield and reduced draught power.
During a severe outbreak in Kolhapur (Maharashtra), India, in 2009, Venkatesan et al. (2010) reported a loss of approximately 40% in terms of reduced milk production and a decline in animal trade. Bhanuprakash et al. (2010) reported that in four outbreaks in India during 2006-2008 there was a significant reduction in milk yield (30-35%) of affected animals, and in some cases, there was a permanent reduction in milk yield as a sequel to severe mastitis. The estimated cost of treatment per animal was approximately US$ 8.5, which corresponds to a 15-20% loss of income per month per animal during the course of the outbreak.
Buffalopox in humans is mainly known from those who have had immediate contact with buffalo, mainly milkers. Those successfully vaccinated against smallpox are protected from infection. However, since the eradication of smallpox and the discontinuation of vaccination, the proportion of susceptible individuals is increasing. The impact of this may now be becoming apparent as it has recently been suggested that outbreaks have become more frequent and that the disease in humans is becoming more severe (Jayaraman, 1996; Tarang Goyal et al., 2013). Some outbreaks have been associated with numbers of cases in individuals who have had no known contact with buffalo, suggesting that human-to-human transmission may now be occurring (Kolhapure et al., 1997).
Animals normally make an uncomplicated recovery. However, affected animals are often treated with antibiotics to prevent secondary bacterial infections (Rani et al., 2006; Debasis Jana and Mousumi Ghosh, 2008; Venkatesan et al., 2010), and antibacterial cream may be applied to the skin lesions (Rani et al., 2006; Debasis Jana and Mousumi Ghosh, 2008).
In countries where the disease is endemic and animal movement is difficult to restrict, disease control is complex. The problem is compounded by lack of precise diagnostics and prophylactics. The contamination of buffalo meat for export is also a problem (Singh et al., 2007).
No specific strategies for control have been described but because transmission is often by contact via milkers, good hygiene practices are recommended for milkers, such as washing hands with antiseptic solutions before and after milking.
Any animals that are clinically affected should be milked last and infected humans should be discouraged from having contact with buffaloes until lesions have resolved. In addition, purchased animals should be carefully examined and if suspect lesions are detected then animals should be isolated until lesions have resolved.
No commercial vaccines are available.
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