Vasculitis Of Arteries Research Articles

NON-TRAUMATIC GRAM-NEGATIVE BACILLARY MENINGITIS IN THE DETROIT MEDICAL CENTER, 1964–1974 (WITH SPECIAL MENTION OF CASES DUE TO Escherichia coli)

Clinical and autopsy records of eight adults with non-traumatic gram-negative bacillary meningitis who were admitted to the hospitals of the Wayne State University--Detroit Medical Center during the years 1964 to 1974 were reviewed. There were five community-acquired cases, and five patients died. Escherichia coli was the causative enteric bacillus in six cases. Community-acquired infections were due to Esch. coli in four of the patients. Each of the patients with a community-acquired infection was a chronic alcoholic. Esch. coli bronchopneumonias, urinary infections, and bacteremias seeding the meninges were usual. Shunting contaminated portal venous blood through the liver in patients with Laennec's cirrhosis, or bypassing the liver with similar infected blood from a genitourinary source by way of Batson's perivertebral plexus draining into the cerebral dural sinuses may be important in the pathogenesis of these infrequent cases of nontraumatic gram-negative bacillary meningitis. Spontaneous gram-negative bacteremias, peritonitis, bronchopneumonias, and now "meningitis" may be a constellation of special complications of the alcoholic. Mortality among 25 patients with Esch. coli meningitis reported from 1922 to 1974 is approximately 50%, and has not changed appreciably during the antibiotic era. Mortality, however, is significantly higher in nosocomially acquired cases. Early and more recent cases have had bloody, xanthochromic pleocytoses indicative of leptomeningeal arterial and venous vasculitis, and far advanced disease. Since causative/enteric bacilli have been susceptible to antimicrobial agents employed, another mode of antibacterial administration, perhaps utilizing parenteral plus intraventricular dosing, particularly for patients acquiring their infections in the hospital, may be required.

Peripheral Corneal Degeneration and Occlusive Vasculitis in Wegener's Granulomatosis

A 61-year-old white woman, who had progressive arthritis over a two-year period, developed bilateral peripheral corneal degeneration. The superior cornea thinned to a thickness of approximately two thirds of normal. She died suddenly in the hospital and a primary occlusive vasculitis of the anterior ciliary arteries within the superior rectus muscles was found. There was necrotizing arteritis in the lungs, kidneys, adrenal caps, spleen, fallopian tubes, and skeletal muscle. The observation of an occlusive vasculitis of the anterior ciliary arteries in this patient supports the belief that ischemia may play a major role in peripheral marginal degeneration of the cornea.

Spectrum of angiographically demonstrable renal pathology in young hypertensive patients.

The renal diseases which cause systemic hypertension in the first two decades of life differ from the adult in their incidence and etiology. Seventeen patients (11 days to 20 years old), studied angiographically, demonstrated a wide spectrum of renal pathology including arterial thrombosis, fibromuscular hyperplasia, vasculitis, neurofibramatosis, cystic disease, pyelonephritis, Page kidney, and congenital anomalies.

Mucocutaneous lymph node syndrome presenting as acute cholecystitis

AbstractMucocutaneous lymph node syndrome (MLNS) is not uncommon in Japan and it is well recognized that the dominant lesion is located in the coronary artery. We experienced recently a particular case which was diagnosed at first as acute cholecystitis, but a definite diagnosis of MLNS was later made from clinical manifestations and laboratory findings, especially ECG tracings, selective coronary angioram and selective celiac angiogram. We discussed the significant relationship between acute cholecystitis and MLNS.Mucocutaneous lymph node syndrome (MLNS) is an acute febrile and eruptive disorder described by Kawasaki1)2) for the first time in 1967. According to increasing reports, it has become gradually clear that the dominant lesion is located in the coronary artery and the symptoms result from the generalized vasculitis in small arteries and arterioles. Its etiology, however, remains unknown.The case, presented here was diagnosed at first as acute cholecystitis and treated with antibiotics, but a definite diagnosis of MLNS was later made by ECG and coronary angiograms.

Skin lesions in human yersiniosis. A histopathological and immunohistological study.

Various types of skin manifestations of human yersiniosis were examined with routine histological and immunohistological methods. The biopsy material consisted of sixteen cases of erythema nodosum, eight cases of erythema multiforme, and one case of erythema figuratum. The principal histopathological changes in erythema nodosum were septal or diffuse, mild panniculitis and in seven cases also necrotizing vasculitis in small, medium-sized or large arteries. Perivascular lymphocytic infiltration without vasculitis was the most prominent feature in erythema figuratum. By using a polyvalent conjugate, immunoglobulins in vessel walls in the dermis were found in two cases of EM. The rapid course of the skin eruptions and the frequency of necrotizing vasculitis in arteries fit the changes seen in an experimental Arthus reaction, in which necrotizing vasculitis is followed by lymphocytic inflammation consistent with a delayed type of reaction.

Letter: Temporal arteritis and pulmonary emboli.

To the Editor. —I am presently preparing a paper on giant cell arteritis and read with interest an article by Stanley A. Uriu, MD, and Robert D. Reinecke, MD, in the November 1973 issue of theArchivestitled Temporal arteritis, steroid therapy, and pulmonary (90:355, 1973). These authors suggested that the treatment of this disease with high dose steroids may have a relationship to the pulmonary emboli supposedly verified in these cases. I cannot refute their theory, but I would like to suggest that these two patients may have had a vasculitis of the pulmonary arteries causing these symptoms, which are identical to pulmonary emboli seen in patients with systemic lupus erythematosus (SLE). I have recently observed such a case. I was initially quite confident with results of lung scans and clinical laboratory evidence that the patient indeed had multiple recurrent pulmonary emboli. She had been receiving anticoagulation therapy,

Penicillium viridicatum mycotoxicosis in the rat. II. Scrotal lesions

Necrosis and ulceration of the scrotal epidermis developed in most rats fed cultures or fungal mats of Penicillium viridicatum for 3–6 wk. Advanced lesions were characterized by a severe necrotizing cellulitis of the epididymal adipose connective tissue and the scrotal fascia surrounding the tunicae and were accompanied by necrosis and ulceration of the epidermis. The progression of scrotal lesions was followed in a sequential study in which five rats were killed daily from day 3 to day 24 of the feeding of a 25% fungal diet. The earliest changes occurred in the epididymal connective tissue as small focal accumulations of leucocytes, usually located perivascularly. Later, multiple loci of necrotic leucocytes accompanied by vasculitis of small arteries and veins appeared in the epididymal connective tissue. As the lesions increased in severity, loci of necrotic leucocytes developed in the connective tissue on the outside of the tunicae. Enlargement and coalescence of these foci produced lakes and bands of necrotizing cellulitis in the scrotal subcutis. Necrosis and ulceration of the epidermis occurred late in the sequence of changes. The same developmental pattern of scrotal necrosis occurred in rats fed fungal mats. Extrascrotal skin lesions involving the back, tail and pelvic limbs were observed in rats fed fungal cultures for 6–8 wk.

NECROTIZING VASCULITIS WITHOUT VISCERAL INVOLVEMENT

Abstract The biopsy and postmortem findings are reported in three elderly patients with a widespread necrotizing vasculitis of the small arteries and arterioles of muscles and peripheral nerves and no clear involvement of visceral organs. Most of the affected vessels had a diameter between 50 and 200 μ. Two of the cases also had a temporal arteritis and the third had a vasculitis of the small vessels surrounding the temporal artery. All cases showed fibre loss in the peripheral nerves, probably caused by ischaemic nerve lesions, and widespread denervation atrophy of the muscles. On the whole the nerves and muscles of the legs were most severely affected.All cases had attacks of fever, high erythrocyte sedimentation rate, and increased globulin fractions in the serum, and all cases appeared to improve to some extent on steroid treatment. The clinical picture had features in common with temporal arteritis and polymyalgia rheumatica. It is emphasized that elderly patients with such symptoms may develop signs of neuropathy during the course of the disease, which is due to a vasculitis of small vessels. This vasculitis may remain localized to muscles and peripheral nerves.

WEGENER'S GRANULOMATOSIS AND CORNEO-SCLERAL ULCER.

To the Editor:— Wegener's granulomatosis is a rare collagen disease of unknown etiology originally described by Klinge. 1 Wegener 2 was the first to correlate the findings into a specific entity distinct from periartertis nodosa. Since then little has been added to basic knowledge of the etiology or pathogenesis of this disease. The usual clinical picture has been well outlined by Fahey. 3 There is no predisposition for either sex. Age varies greatly, but is usually in the third to fifth decade. The onset is heralded by upper-respiratory-tract symptoms, most often nasal stuffiness and sinusitis. Abnormal pulmonary findings, fever, and weight loss follow, and the course progresses unfavorably, ending with renal failure as a rule. McDonald 4 characterizes the three salient findings as a necrotizing granulomatous process of the respiratory tract, a generalized vasculitis of the arteries and veins, and focal glomerulitis. 5 To our knowledge only five previous documented

Experimental arterial sensitization: Studies on the specificity of “shock tissue”

1. 1. Albino rabbits of the same strain and approximate age and weight were passively sensitized with homologous antiserum to and challenged with horse serum according to a procedure favoring the production of acute lesions of vasculitis of the pulmonary arteries, arterioles, and veins. 2. 2. Of ten animals sensitized and challenged intravenously through the ear vein, all developed the typical lesions of periarterial infiltration consisting chiefly of eosinophils and polymorphonuclear leukocytes and, to a much lesser extent, lymphocytes and mononuclear cells with some eosinophilic infiltration into the adventitia, media, and intima of the small pulmonary arteries and arterioles. The vasculature of other organs was unaffected. 3. 3. Of nine animals subjected to similar procedures via the intracarotid arterial route, six developed similar pulmonary lesions, but the lesions were of milder intensity and were less frequently found than those sensitized and challenged by the intravenous route. The brains of these rabbits were free of lesions. 4. 4. Eight animals received similar sensitizing and challenging injections intraperitoneally. In this group, lesions suggesting pulmonary vasculitis were infrequently found and were of a very mild or equivocal degree. Lesions could not be demonstrated within the liver following this procedure. 5. 5. These results suggest that although modified by the route of administration of sensitizing and challenging doses, the development of acute lesions of pulmonary vasculitis may depend upon some undetermined specificity of the rabbit lung in participating in antigen-antibody reactions not found in the brain or liver of this animal. 6. 6. Although not apparent, the reason for the involvement of the pulmonary vasculature in this reaction, considered a tissue manifestation of subacute anaphylaxis, may be related to the role of the pulmonary arteries as “shock organ” in anaphylactic shock.