Adam Ewert

The effect of streptococcus on the persistence of Brugia malayi and on the production of elephantiasis in cats

Abstract Cats were exposed to 200 Brugia malayi larvae on one hind foot over a 3 week period. Six weeks after the initial exposure to B. malayi , 10 of the cats were challenged on both hind legs with a Group G streptococcus. The remaining 10 cats were not exposed to the streptococcus. Following bacterial challenge, the B. malayi -infected leg of 9 of 10 cats displayed sequelae including erysipelas and abscesses. In addition, 5 of the affected legs had an elephantoid appearance, both by gross observation and as seen at necropsy 10 weeks after the initial B. malayi infection. The contralateral, uninfected leg of each cat remained normal in appearance. Histologic processing and examination of the elephantoid tissue showed it to be collagen; eosinophils and mast cells were plentiful in the collagen matrix. In the controls, only 1 animal displayed erysipelas and no abscesses were seen. Lymphedema seen in the B . malayi -infected leg of 5 control cats was less extensive than in uninfected cats challenged with streptococci and at necropsy no significant collagen matrix was evident. The location and number of worms in the lymphatics were noted. This study demonstrated that secondary microbial infections can contribute to the causation of elephantiasis under certain circumstances and that developing B . malayi were in some way adversely affected by the streptococcal involvement of the filaria-infected lymphatics.

Degenerative Changes in Lymphatic Endothelium of Jirds Infected with Brugia pahangi

The quantitative changes of cytoplasmic vesicles and vacuoles in lymphatic endothelial cells of the mongolian jirds associated with Brugia pahangi infections were observed by transmission electron microscopy. The present study revealed a decrease in the proportion of cytoplasm occupied by vesicles and in the number of cytoplasmic vesicles in endothelial cells from lymphatic vessels harboring B. pahangi at 3, 4, and 10 mo after infection (3.55, 3.36, and 2.55 vesicles/micron 2, respectively) when compared with cells from uninfected control vessels (7.03 vesicles/micron 2). On the contrary, there was an increase in the area of vacuoles in endothelial cells of jirds at 3, 4, and 10 mo postinfection. The mean +/- SD diameter of vesicles in cells from lymphatic vessels at 10 mo after infection was significantly smaller (78.6 +/- 5.6 nm) compared to vesicles in uninfected vessels (87.5 +/- 9.7 nm).

COLLAGEN METABOLISM IN EXPERIMENTAL FILARIASIS

Chronic lymphatic filariasis is accompanied by edema and fibrosis. In order to assess the latter response, the tissue content of collagen was measured in the skin and lymphatic vessels of normal and affected limbs of cats infected by Brugia malayi. Collagen content, expressed per gram wet weight of tissue, was increased in the infected limbs for both kinds of tissues. Moreover, the proportion of acetic acid soluble to total collagen was increased. The degree of crosslinking in soluble collagen was assessed by acrylamide gel electrophoresis and shown to be decreased in infected tissues. These data suggest an increased rate of collagen metabolism in Brugia malayi-infected tissues and provide data for future studies evaluating the efficacy of treatment in chronic experimental filariasis.

Experimental necrotic dermatosis induced by group G streptococci in mice

SummarySelf healing necrotic lesions were produced on the backs of laboratory mice by injecting group G streptococci into the skin. The incidence and severity of necrotic dermatosis was dose related. When 1×101 colony forming units (cfu) were injected subcutaneously, lesions developed on three of 16 mice 4 days post inoculation. Injection of 1×103 cfu produced lesions on five of 16 mice and 1×105 cfu produced lesions on seven of 15 mice 3 days post inoculation. An inoculation of 1×107 cfu produced lesions on all of 16 mice 2 days post inoculation. Lesions produced by the 1×101 inoculum were smaller and had healed by the 15th day post inoculation, whereas lesions produced by the 1×107 inoculum persisted until the 24th day post inoculation. No mortality could be attributed to experimental design and all lesions healed without the use of medication or antibiotics.

Distribution and development of Brugia malayi in reinfected cats.

At various time periods after an initial exposure to 50 Brugia malayi larvae on one hind foot cats were reexposed to an additional 50 larvae in one of 3 ways: on the previously infected limb only, on the contralateral, uninfected limb only, or on both hind limbs simultaneously. At the time of reexposure uninfected controls were exposed to 50 larvae on one hind foot in a similar manner. From 2 to 4 weeks after reexposure to larvae, the cats were necropsied and the appropriate lymph nodes and vessels examined for adult or developing worms. An existing infection in one limb did not influence early migration or development of larvae introduced into the contralateral leg. Previous infection in the same limb did not consistently result in decreases in the number of developing larvae from the second exposure but did alter the distrubution of larvae. In repeat infections, larvae were consistently located in a moe distal area of the limb than were larvae from an initial infection at a comparable time.