Signalment:  

Suckling pig, about 4 weeks of age, female, porcine, breed unspecified (Sus domestica)Reduced weight gain within the herd. Suckling pigs show heavy breathing and die unexpectedly.

Gross Description:  

Multiple tongue erosions, yellowish secretion from the nose, yellowish plaques on nasal turbinates.

Histopathologic Description:

Nasal turbinate: Diffusely, the subepithelial connective tissue is expanded and infiltrated by numerous lymphocytes, plasma cells, and fewer macrophages. Epithelial cells of the nasal mucous glands and the respiratory epithelium are multifocally slightly enlarged (cytomegaly) with abundant, foamy, eosinophilic cytoplasm and a single 20-30 μm, basophilic, irregular, smudgy and granular, intranuclear inclusion body (Fig. 4-1) that fills and distends the karyomegalic nucleus. Multifocally the mucous glands are ectactic, lined by attenuated epithelium, and contain variable amounts of eosinophilic cellular and karyorrhectic debris (necrosis) with rare neutrophils. The respiratory epithelium is multifocally lost and replaced by a moderate amount of karyorrhectic and pyknotic cell debris (necrosis). In the nasal passage, there is an exudate composed of erythrocytes, sloughed epithelial cells, and some slightly eosinophilic material (mucous).

There is a large focally extensive necrotic area (not included in every slide), characterized by a large amount of eosinophilic karyorrhectic and pyknotic cell debris, and bordered by an abundant amount of small and medium caliber vessels surrounded by reactive fibroblasts and collagen (granulation tissue).

Morphologic Diagnosis:  

Nasal turbinate: Rhinitis, lymphoplasmacytic and necrotizing, subacute, diffuse, marked, with glandular epithelial karymegaly due to intranuclear inclusion bodies

Lab Results:  

Corynebacterium spp. were isolated from the nasal turbinate.

Condition:  

Porcine cytomegalovirus (inclusion body rhinitis)

Contributor Comment:  

Inclusion body rhinitis porcine cytomegalovirus (PCMV) PCMV infections are ubiquitous and occur throughout the world, but clinical disease is much less frequent. Inclusion body rhinitis is typically an acute to subacute disease of 3-5-week-old suckling piglets. Piglets exhibit fever, sneezing, catarrhal nasal exudate, shivering, and occasional dyspnoe. Morbidity is high and mortalitiy is low unless secondary bacterial infections develop. Systemic cytomegalovirus infections usually infect piglets less than 3 weeks of age. These piglets may be found dead without premonitory signs, or exhibit sneezing, lethargy, anorexia, subcutaneous edema of the jaw and tarsal joints, and dyspnea. Infection of na+�-�ve pregnant sows induces mild lethargy, anorexia, and delivery of stillborn or weak piglets. Inclusion body rhinitis is caused by PCMV, a beta-herpesvirus. Piglets commonly shed the virus soon after weaning at 3 weeks of age, suggesting that infection is usually acquired by contact with nasal secretions of infected cohorts. Other pigs, particularly those that develop generalized disease, are probably infected from the sow in the neonatal period. The virus replicates in nasal submucosal and lacrimal glands. Viremia develops at 5-14 days after infection depending on the age of the pig and leads to infection of epithelial cells in renal tubules, liver, duodenum, and elsewhere. Pulmonary alveolar and splenic macrophages may be additional sites of viral replication. Virus is shed in nasal and ocular secretions, in the urine, and in vaginal secretions of sows.(3)

Infection can be diagnosed by the presence of characteristic large, basophilic, intranuclear inclusion bodies in cytomegalic cells of the nasal glandular epithelium. Such inclusion bodies and mononuclear cellular infiltrations can also be detected in the tubular epithelia of the kidneys, as well as the epithelia of the salivary and tear glands. Other, less frequent, lesions include interstitial pneumonia and lymphocytic perivasculitis in the brain. Predisposing factors of the infection are not fully known. A low level of immunity within the herd, e.g., in newly established herds, and immunosuppressive effects may play a role. Seroconversion due to PCMV is probably much more frequent than clinical disease.(1) In our case, sows in the herd had problems with insufficient lactation.

Herpesviridae

Alphaherpesvirinae: focal lesions in skin and mucosa of resp. and genital tract; abortion; neonates: necrosis in multiple organs, latency in nerves	Equine herpesvirus 1: Equine herpesviral abortion, rhinopneumonitis, neurologic disease	horse
	Equine herpesvirus 3: Equine coital exanthema	horse
	Equine herpesvirus 4: Equine rhinopneumonitis	horse
	BHV-1: infectious bovine rhinotrcheitis/infectious pustular vulvovaginitis/infectious balanoposthitis	cattle
	BHV-2: bovine mammilitis virus (bovine herpes mammilitis)	cattle
	BHV-5: bovine herpesvirus encephalitis	cattle
	SHV-1: Aujezky-�s disease, Pseudorabies	pig > others
	Canine herpesvirus 1:	dog
	Feline herpesvirus 1: upper respiratory tract disease (rhinotracheitis) and conjunctivitis (ulcers)	cats
	Feline herpesvirus 1: feline herpesvirus ulcerative dermatitis	cats
	Gallid herpesvirus-1: Infectious laryngotracheitis (ILT)	chicken
	Gallid herpesvirus-2: Marek-�s disease	chicken
	Psittacine herpesvirus: Pacheco's disease	psittacines
	Anatid herpesvirus-1: Duck plaque/Duck virus enteritis	ducks, geese, swan
	Simplexvirus: HSV-1, HSV-2, HBV, BHV-2
	Herpesvirus simplex, type 1/type 2	human & nonhuman primates
	Herpesvirus simiae/Herpes B/Cercopithecine HV	rhesus macaques
	Simian varicella virus	macaques, AGM, Patas monkeys
Betaherpesvirinae: no cell lysis, karyomegaly, latency in secretory glands, lymphoreticular organs, kidney	HHV-5, HHV-6, MCMV-1	humans
	Porcine herpesvirus 2: porcine cytomegalovirus disease/Inclusion body rhinitis	porcine
	Cytomegalovirus	humans & nonhuman primates
Gammaherpesvirinae: primates: lymphoproliferative disease, latency in lymphoid tissue	EHV-2
	EHV-5
	BHV-4: bovine herpes mammary pustular dermatitis	cattle
	OHV-2/AHV-1: malignant catarrhal fever	various ruminants
	Epstein-Barr virus (lymphocryptovirus-gamma 1)	primates
	Kaposi-sarcoma-associated herpesvirus/human herpesvirus-8 (KSHV/HHV8) (Rhadinovirus-gamma 2)	primates
Deltaherpesvirinae	Anatid herpesvirus-1: duck plague
	SHV-2: Eischlussk+�-�rperchenkrankheit	pig
	Karpfenpocken	fish
Uncharacterized viruses	Koi-herpesvirus (KHV, carp nephritis and gill necrosis virus, CNGV, Cyprinid-Herpesvirus-3, CyHv-3)	fish

JPC Diagnosis:  

1. Nasal turbinates: Rhinitis, necro-ulcerative, subacute, diffuse, moderate, with glandular epithelial eosinophilic intranuclear inclusions
2. Haired skin and bone: Necrosis, focally extensive, with granulation tissue, fibrosis, osteonecrosis and osteolysis

Conference Comment:  

The contributor provides a comprehensive summary of this condition. One additional rule-out considered by attendees was atrophic rhinitis; however, changes in the nasal turbinate cartilage and bone would be an expected finding, as well the absence of inclusion bodies. For comparison purposes, a brief discussion of atrophic rhinitis is included here. Atrophic rhinitis is also a common disease in pigs worldwide. Atrophic rhinitis can be split into nonprogressive atrophic rhinitis (NPAR), caused by Bordetella bronchiseptica, or progressive atrophic rhinitis (PAR), caused by toxigenic Pasteurella multocida as a single agent or in combination with Bordetella bronchiseptica. Both of these disease cause hypoplasia of the nasal turbinates that clinically manifest as frequent sneezing by affected swine. Progression of either of these diseases can lead to distortion of the snout. Nasal hemorrhage is commonly seen in PAR; NPAR nasal hemorrhage is uncommon.(2)

Both Bordetella bronchiseptica and Pasteurella multocida produce their own toxins, and the severity of disease is dependent on the amount of toxin absorbed. One major difference between these two organisms is the age of affected pigs. PAR can affect pigs older than 3 months of age, whereas NPAR normally only affects pigs up to 6 weeks of age.(2)

Gross lesions in PAR are restricted to the nasal cavity and adjacent bone with the ventral scrolls of the nasal turbinates most often suffering the worst lesions. Histologically, the pathognomonic lesion of PAR is replacement of the bony plates of the ventral conchae with fibrous tissue. Metaplasia of adjacent respiratory epithelium is also common.(2)

References:

1. Deim Z, Glavits R, Biksi I, Dencso L, Raczne AM: Inclusion body rhinitis in pigs in Hungary. Vet Rec. 158(24):832-4, 2006
2. De Jong MF:Progressive and nonprogressive atrophic rhinitis. In: Diseases of Swine, ed. Straw BE, Zimmerman JJ, DAllaire S, Taylor DJ, 9th ed., pp.577-602. Blackwell Publishing, 2006

Click the slide to view.

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4-1. Nasal turbinates, pig

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