Dermatitis and nephropathy syndrome

From Pig

Porcine dermatitis and nephropathy syndrome (PDNS) is a rare immune-mediated disease of pigs.

PDNS was first described in Chile in 1976 under the name proliferative glomerulonephritis in young pigs. Since then the sporadic form of this disease has been widely reported from all pig-producing areas around the world. It has become prevalent since the occurrence of postweaning multisystemic wasting syndrome (PMWS), although its link with porcine circovirus type 2 (PCV2), considered the causal agent of PMWS, has not been definitively proved.

PDNS is characterized by vasculitis in many organs, particularly the skin and kidneys, with resulting clinical signs. The pathologic changes of PDNS suggest an immune complex disorder, with severe renal lesions causing azotemia that results in the death of affected pigs, usually in the growing and finishing areas. The incidence of PDNS is generally low (<1%), but during the late 1990s, an epizootic version of PDNS, which was clinically and macroscopically very similar to classical swine fever or African swine fever, was reported in the UK[1].

Cause

PDNS occurs in all types of swine production systems with different health status and management procedures. Disease presentation tends to be sporadic with incidence <1%; however, incidence of up to 10-20% or even higher (epizootic presentation) has been described. Most reports suggest that PDNS appears without any changed management, husbandry, or dietary practices. Many other diseases, clinical signs, and gross lesions appear to coincide with occurrence of PDNS, including PMWS, porcine reproductive and respiratory syndrome (PRRS), conjunctivitis, gastric ulcers, and a variety of respiratory, digestive, and systemic bacterial infections.

Microscopic lesions of PDNS strongly suggest an immune complex-mediated disease. Immunoreactants such as IgM, IgA, and occasionally IgG, and complement factors C3 and C1q, have been detected within renal glomeruli and affected vessel walls. However, the responsible antigen(s) involved in the immune complex-mediated disorder is currently unknown, and several etiologic possibilities have been postulated. PCV2, PRRS virus, and Pasteurella multocida are the most studied, but the definitive role of any of these antigens in the disease pathogenesis has not been determined. More recently, PCV2 has been further indirectly linked to PDNS because the affected pigs have extremely high levels of PCV2 antibodies.

Clinical signs

The disease usually has an acute onset in a single pig or in a group of pigs. Multiple or coalescing skin lesions occur in ~90% of cases. Cutaneous manifestations, however, may vary and may be confused with classical and African swine fever, swine erysipelas, septicemic salmonellosis, infection with Actinobacillus suis , porcine stress syndrome, transit erythema (urine-soaked floors, chemical burns, etc), and other bacterial septicemias. Affected pigs typically weigh 25-70 kg. Morbidity is usually <1% but may be 0.05-30%; case mortality is usually 80-90%. Often there is a short clinical illness (a few hours to 3 days), with some sudden deaths. Pigs with skin conditions usually die despite treatment. Many pigs are pyrexic (up to 41.5°C) with anorexia and listlessness; some are depressed, prostrate, or unwilling to stand or move. Many pigs have edema of the lower limbs and ventral body surfaces. A few pigs with skin lesions survive, with resolution of the lesions (as scars) over 2-3 wk. Some pigs show very mild effects, which may range from a vague malaise to more obvious illness with reduced feed intake and weight loss; those pigs with milder clinical signs usually have no or only slight kidney lesions.

The skin lesions are the most striking feature but are not always present. They may be multifocal, flat, discrete lesions (1 cm or less) with an irregular margin, but are more commonly seen as larger, coalescing lesions on any part of the body. Lesions are usually worse on the hindlimbs, perineum, ventral abdomen, and flanks. Erythema may be intense, giving a rosette appearance on close inspection. Occasionally the skin lesions turn purple or black, signalling the onset of dermal necrosis. In some animals, blackened skin across the rear and perineum develops and may even ulcerate; these pigs always die.

In addition to skin lesions, gross necropsy findings include enlarged kidneys with petechial hemorrhages in the cortices, enlarged and congested lymph nodes, excess fluid in body cavities, serosal surface and subcutaneous hemorrhages, and serosanguineous fluid in joint cavities. Other lesions, such as cranial lung lobe pneumonia, hyperkeratosis and ulceration of the stomach, and pericarditis, are considered features of concurrent diseases or conditions.

Histopathologic findings are essentially those of a systemic necrotizing vasculitis with hemorrhage, edema, and fibrinoid necrosis, affecting medium- and small-sized arteries of many tissues (virtually all vascularized tissues may be affected). Kidney lesions vary from a marked, acute, fibrinous glomerulitis with hyaline casts in the tubules and some degree of interstitial nephritis (acute cases) to glomerular sclerosis, nonsuppurative interstitial inflammation, and fibrosis in pigs that survive the acute phase and develop chronic lesions.

Diagnosis

Definitive diagnosis is based on histopathologic findings. There are 2 major criteria for diagnosis: the presence of compatible gross lesions in skin and kidney, and the presence of systemic necrotizing vasculitis and fibrinous glomerulitis. Serum analyses may help differentiate PDNS from other diseases such as classical and African swine fever; in PDNS, urea (normal 8.2-24.6 mg/dL) and creatinine (normal 69.6-207.7 mmol/dL) are markedly increased. Serum globulins (mainly γ-globulins) also increase, and proteinuria is pronounced in all cases. There are no etiologic diagnostic laboratory tests, as no definitive agent has yet been determined.

Treatment

No treatment has proved successful. Rapid hospitalization and supportive care may enable a few affected pigs to survive. Only those epizootic PDNS cases with moderate to high morbidity and mortality rates may be of importance in terms of economic losses. Treatment using a wide range of antimicrobial agents has been unsuccessful. Some field experiences have suggested that the use of anti-inflammatory drugs and multivitamin supplements to control PDNS and PMWS, together with the minimization of stress factors, may be of benefit.

Because the pathogenesis of PDNS is not known, no preventive recommendations have been indicated to be of value in control.

References