Elektronenmikroskopische Untersuchungen des Keratoakanthoms

Bülow, M.; Klingmüller, G

doi:10.1007/bf00595445

Cited by 25 publications

(1 citation statement)

References 14 publications

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“…Viral induced membrane lesions probably caused permeability changes and sub- sequent cellular separation. Other acantholytic mechanisms are (1) activation of complement by properdin or C3 proactivator (C3PA) as reported in herpes gestationis, systemic lupus erythematosus, and bullous pemphigoid [18] and pemphigus [12]; (2) desmosomal dedifferentiation as described in wool follicles [ 161 ; and (3) destruction of glycocalyx by enzymes from neutrophilic or keratinocytic lysosomes. Whorls of tonofilaments were not present in the cytoplasm of infected keratinocytes as reported in pemphigus [9, 24, 251, nor in familial acantholysis of Angus calves [l 11.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural Changes in Bovine Lingual Epithelium Infected with Vesicular Stomatitis Virus

Proctor

Sherman

1975

Vet Pathol

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Abs/r.ac/. Vesicular stoniatitis virus was inoculated into the dorsal lingual epithelium of three cows. The reaction that developed in 72 h was characterized by severe acute diffuse glossitis with intercellular edema and necrosis of keratinocytes. Virions budded from the plasma membrane and were in the intercellular spaces. Reduplication of desmosomes was a prominent alteration, and normal desmosomes were within the cytoplasm. Intracytoplasmic desmosomes appeared to be formed by endocytosis after breaks occurred in the plasma membrane of one cell; endocytosis of loops of plasma membrane containing desmosomes; and formation of desmosomes on invagination of the plasma membrane. Vesicular stomatitis is caused by rhabdovirus, which naturally affects cattle, horses and swine and produces vesicular lesions in the epithelium of the tongue, gingiva, lips, teats, coronary bands, interdigital spaces and snout. Gross lesions begin as small papules that become hyperemic and rapidly develop into vesicles that coalesce to form bullae. Normal movement of the skin causes bullae to rupture and form erosions or, occasionally, ulcers. Intercellular edema in the stratum spinosum is an early change and leads to acantholysis and vesicle formation [3, 4, 221. RIBELIN [I91 found similar histologic lesions in bovine lingual organ culture infected with vesicular stomatitis virus and concluded that intercellular edema was not secondary to vascular damage.

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Section: Discussionmentioning

confidence: 99%