Lumpy Skin Disease: A Rising Threat to Cattle Health and Livelihoods
Dr. Manisha , Dr. Preeti Godara
1. Teaching Associate , PGIVER, Jaipur
1. Assistant Professsor, Department of Veterinary Microbiology
Abstract
Lumpy Skin Disease (LSD) is an economically significant viral disease affecting cattle and buffaloes, characterized by the emergence of skin nodules and systemic clinical signs. The causative agent, Lumpy Skin Disease Virus (LSDV), belongs to the Poxviridae family and is closely related to capripoxviruses such as sheep pox and goat pox viruses. The disease has devastating effects, including reduced milk production, infertility in bulls, abortions in pregnant cows, and permanent damage to animal hides. LSD primarily spreads through biting insect vectors like mosquitoes and flies, though direct contact with infected animals’ bodily fluids is also a potential route.
Clinical signs of LSD vary widely, from mild to severe, with lesions affecting various body parts. Gross pathological findings reveal full-thickness skin nodules, necrosis, congestion, and subcutaneous fat depletion. Affected lymph nodes, lungs, liver, and kidneys exhibit marked changes, including hemorrhages, edema, necrosis, and mononuclear infiltration. Microscopic examination highlights hydropic degeneration, ballooning of epidermal cells, and eosinophilic inclusion bodies in affected tissues. The liver shows fatty degeneration and necrosis, the heart displays epicardial thickening and vasculitis, while the lungs and kidneys exhibit congestion and degenerative changes.
Despite its economic and veterinary importance, the pathogenesis and host immune response to LSD remain poorly understood, necessitating further research. Understanding these mechanisms is crucial for developing effective control and prevention strategies, particularly in regions like Asia, where outbreaks since 2019 have caused significant cattle mortality.
Keywords: LSD , Histopathology,
Introduction
During the summer and monsoon months of 2022, a significant loss of animal life occurred due to the spread of Lumpy Skin Disease Virus (LSDV).Lumpy Skin Disease Virus (LSDV) belongs to the Poxviridae family, with the Neethling strain as its prototype. It is part of the Capripoxvirus genus, which also includes the sheep pox and goat pox viruses.LSDV leads to a temporary or permanent decline in milk production, reduced fertility or sterility in bulls, occasional abortions in pregnant cattle, and lasting damage to animal hides.Most earlier studies focused on the skin lesions caused by LSDV, with limited emphasis on its effects on other organs such as superficial lymph nodes, skeletal muscles, the udder, and testes.LSDV is present in skin nodules, crusts from skin lesions, as well as in blood, saliva, nasal discharge, semen, and milk (Babiuk et al., 2008).Lumpy skin disease (LSD) is an emerging viral disease of economic importance in cattle and buffaloes, marked by the formation of skin nodules (Möller et al., 2019).Since 2019, the Asian continent has faced significant outbreaks of the disease, with multiple incidents reported, including in India (Manjunatha Reddy et al., 2023).The incubation period of the disease varies from 7 to 35 days in naturally transmitted infections. Clinically, it presents with symptoms such as fever, firm, flat-topped, well-defined papules and nodules of different sizes on the body, lymphadenopathy, and edema in the limbs, abdomen, and brisket area. Typically, after 2-3 weeks, the nodules become necrotic, forming characteristic ‘Sit-fast’ sequestrum of necrotic material (OIE 2024).The pathogenesis of Lumpy Skin Disease (LSD), particularly the immunopathological changes in skin nodules and the host’s immune response to natural LSDV infections, is not well understood. To date, there has been no research on the LSDV-induced pathology, virus distribution, or viral load in the skin and internal organs during the recent LSD outbreaks in Indian cattle, which led to high mortality. It is well established that effective antiviral defenses involve both innate and adaptive immune responses, including apoptosis (Birge and Ucker 2008).
Transmission
The primary mode of transmission for the causative pathogen is through biting insects, such as mosquitoes and biting flies, which act as vectors. Direct contact with skin lesions, milk, nasal discharge, saliva, or semen from infected animals is a less common route of transmission.
Pathogenesis
The precise mechanisms underlying lesion development in multiple organ systems caused by LSD remain unclear. However, it is suggested that the tissue tropism and viral shedding in LSD may share similarities with capripoxvirus infections in sheep and goats.
Clinical signs
Cattle infected with LSDV, either experimentally or naturally, exhibit a wide range of clinical signs, varying from minimal symptoms to severe, widespread lumpy skin disease. The severity of signs ranged from mild to severe, with cutaneous lesions appearing as papules that developed into nodules of varying sizes (0.5–3 cm in diameter). These eventually formed scabs, which could either slough off, leaving ulcers, or heal, affecting most of the skin surface, including the head, neck, shoulders, inguinal region, genital organs, and limbs (Fig. 1) these lesions were accompanied by general symptoms such as fever, loss of appetite, salivation, ocular nasal discharge ( fig. 2) and enlarged superficial lymph nodes, with or without corneal opacity and emaciation, often leading to death or emergency slaughter. The skin lesions varied in size and penetrated the full thickness of the skin. The areas with nodules showed congestion, hemorrhaging, and necrosis. Subcutaneous fat displayed varying degrees of serous atrophy, with affected tissues appearing yellowish and gelatinous due to fat depletion. Superficial lymph nodes, particularly the prescapular and prefemoral nodes, were swollen, edematous, and showed multifocal hemorrhages. Necrotic lesions were found on the tongue, tracheal mucosa, larynx, and the serosal surfaces of the rumen, reticulum, abomasum, and gallbladder. Lesions on the rumen, reticulum, and abomasum were erythematous, either circumscribed or irregular, with central pale necrotic areas surrounded by hyperemic margins. The lungs exhibited multifocal patches of consolidation,appearing dark, congested, and firm to touch. In some cases, the liver and kidneys were slightly enlarged and showed discrete multifocal necrotic foci.
Fig. 1 Photograph of lumpy skin disease affected cattle showing nodules of varying sizes distributed all over the body
Fig. 2 Photograph of lumpy skin disease affected cattle showing ocular and nasal discharge
Gross lesions
In necropsied cases of LSD, the skin lesions varied in size and penetrated the full thickness of the skin. The affected areas showed congestion, hemorrhage, and necrosis on the inner surface. Subcutaneous fat exhibited varying degrees of serous atrophy, causing the areas to appear yellowish and gelatinous due to fat depletion. Superficial lymph nodes, particularly the prescapular and prefemoral, were swollen, edematous, and displayed multifocal hemorrhages. Necrotic lesions were found on the tongue, tracheal mucosa, larynx and serosal surfaces of the rumen, reticulum, abomasum, and gallbladder. Lesions in the rumen, reticulum, and abomasum were erythematous, with either circumscribed or irregular borders, a central pale necrotic area, and a surrounding hyperemic zone. The lungs showed multifocal areas of consolidation that were congested (fig.3), dark, and firm to the touch. In some cases, the liver and kidneys were slightly enlarged and contained discrete necrotic foci. Grossly, infected animals showed nodular lesions on the skin of various areas of the body. These lesions were primarily seen on the head, neck, legs, tail, udder and perineum. The lesions were also noticed on the vulval lips, the inguinal region, the muzzle, the lips and the nostrils (fig. 1). In less severely affected animals, the nodular lesions were limited to certain parts of the body.
Fig. 3 Photograph of lumpy skin disease affected lung showing severe congestion
Microscopic lesion
Cattle affected by lumpy skin disease showed hydropic degeneration of the epidermis, particularly in the stratum spinosum and basal cell layer. In some of the examined deceased cases, ballooning degeneration of the stratum spinosum was observed, with the formation of microvesicles filled with serofibrinous exudates. Skin biopsies from infected animals, as well as skin samples from deceased animals, revealed numerous eosinophilic inclusion bodies within the cytoplasm.
Lung
The lungs exhibited intense congestion, hemorrhages, and edematous fluid accumulation in the alveoli and bronchioles.he section of lung showed ballooning/hydropic changes in alveolar wall
Kidney
Kidneys showed congestion and degeneration of tubular epithelial cellsRenal tubules contained eosinophilic proteinaceous cast and degeneration of tubular epithelial cells.
Liver
Severe fatty degenerative changes, necrosis, and infiltration of mononuclear cells were noticed
Heart
The heart displayed thickening of the epicardium with connective tissue proliferation, along with vasculitis, perivasculitis, and infiltration of macrophages.
Conclusion
Lumpy Skin Disease is a severe, multifaceted disease with systemic clinical and pathological manifestations, posing a serious threat to cattle health and the livestock economy. The disease’s ability to compromise multiple organ systems underscores the need for enhanced diagnostic, therapeutic, and preventive measures. A deeper understanding of its pathology, transmission, and immunological aspects will pave the way for improved control strategies, safeguarding animal welfare and livelihoods globally.
Acknowledgment
I would like to sincerely thank my guide, Prof (Dr.) Manisha Mathur from the College of Veterinary and Animal Science (CVAS), Bikaner, for providing financial support and the necessary laboratory facilities for this study.
References
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