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At least 19 recordsLinked to original sources
PubMed1975

The fate and migration of microfilariae of a Guatemalan strain of Onchocerca volvulus in Simulium ochraceum and S. metallicum, and the role of the buccopharyngeal armature in the destruction of microfilariae.

The migration and fate of microfilariae of a Guatemalan strain of Onchocerca volvulus in Simulium ochraceum and S. metallicum was studied. The anatomical distribution of microfilariae at various times after ingestion was recorded from a study of histological sections of the flies. S. ochraceum showed higher microfilarial intakes than S. metallicum which is probably attributed to an inherent difference in their ability to ingest. The migration of microfilariae out of the mid-gut took place essentially through the expanded part (the stomach). Despite the high microfilarial intakes by S. ochraceum, only a few microfilariae were able to migrate successfully into the thorax (2.6%) whereas in S. metallicum showing a low microfilarial intake, a higher rate of migration was noted (74.5%). The main bulk of microfilariae ingested by S. ochraceum died and disintegrated in the stomach. This was due to the presence of a well-developed cibarial armature in the buccopharyngeal apparatus of S. ochraceum in contrast to S. metallicum where such an armature is lacking. Microfilariae were severely damaged by the cibarial teeth while en route to the stomach. They rapidly underwent profound changes in morphology and staining properties and were often surrounded by clusters of the phagocytic leucocytes in the blood mass. In some flies, microfilariae, apparently damaged, were still entangled in the cibarial teeth 5 minutes to 3 hours after taking a blood-meal.

Animals↗
PubMed1977

The microfilaria of Brugia timori (Partono et al. 1977 = Timor microfilaria, David and Edeson, 1964): morphologic description with comparison to Brugia malayi of Indonesia.

The microfilaria of Brugia timori was compared with microfilariae of Indonesian strains of periodic and subperiodic Brugia malayi using alcohol-fixed (stained) and formalin-fixed (unstained) preparations. As noted by other observers of the Timor microfilaria, the absence of a stained sheath in Giemsa preparations, a long cephalic space with a length-to-width ratio of about 3:1, and a great overall body length are features which most readily distinguish this parasite. Additionally, B. timori has greater numbers of single row nuclei in the terminal column of body cells and a lesser bulge of the cuticle surrounding nuclei in the distal portion of the tail than does B. malayi. About 60% of B. timori microfilariae were exsheathed in haemalum-stained thick blood films. Brugia timori microfilariae were found to be distinct from microfilariae of B. malayi by comparing percentages of total body length included between the cephalic tip and major internal anatomic markers.

Animals↗
PubMed1978

[Experiments in vitro with Litomosoides carinii (Nematoda: Filarioidea). I. Maintenance of adult females and microfilariae as well as release of microfilariae in different culture media (author's transl)].

Embryos of L. carinii continue intrauterine development to microfilariae and are totally released into the medium within 5--6 days when the latter (Tc 199) is changed daily and air is used as the gas phase. Oogenesis or further fertilization of eggs, however, does not occur in vitro in any of the media examined by us. One female releases 140 X 10(3) microfilaria/day on an average in vitro within 5--6 days. Mean initial numbers of 300 X 10(3) Mf/female/day are observed. Addition of equine serum inhibits microfilarial release in vitro; normal cotton rat serum prolongs survival of females while total numbers of released microfilariae or retained embryonic stages are not increased. The serum of post-patent animals does not influence the numbers of released microfilariae or their viability or survival of females. Microfilariae released in vitro in Tc 199 + 33% normal cotton rat serum survive for more than 8 days, when air is used as the gas phase and the medium is changed daily. Microfilariae isolated from the blood of patent animals survive for at most 6 days, at a 48-hourly change of medium survival does not even exceed 4 days.

Animals↗
PubMed1976

Transmission of microfilariae and infective larvae of Dipetalonema viteae (Filarioidea) among vector ticks, Ornithodoros tartakowskyi (Argasidae), and loss of microfilariae in coxal fluid.

During studies on the acquisition and transmission of infection with the filaria Dipetalonema viteae by Ornithodoros tartakowskyi, it was found that young nymphs and starved medium-sized ticks feed on recently engorged larger ticks. In this manner young ticks acquired the infection with microfilariae, and the microfilariae thus taken developed normally and after 30 days of development were transmitted to a jird. Ticks harboring infective larvae were able to transfer them to other engorged ticks when attempting to feed on them. Although it is not known whether this occurs in nature, it could be a supplementary mechanism in the natural maintenance of this species of filaria. Ticks eliminated microfilariae in the coxal fluid in small numbers during the 1st hr after the infective meal and in increasing numbers with time, reaching a peak between 3 and 5 hr. This mechanism may prevent some ticks from becoming hyperinfected.

Animals↗
PubMed1990

Acid phosphatase activity in microfilariae of Setaria labiato-papillosa and comparison with other blood microfilariae of dog and horse origin.

Acid phosphatase activity was demonstrated in smears of Setaria labiato-papillosa microfilariae by the naphthol AS-TR-phosphate method. The staining was restricted to 3 distinct sites, corresponding to the excretory pore, the inner body and the anal pore. This staining pattern was compared with those of Dirofilaria immitis, Dirofilaria repens and a Setaria of horse origin.

Acid Phosphatase↗
PubMed1989

Onchocerca gutturosa and Onchocerca lienalis in cattle: variation in length of microfilariae by site of recovery.

Dermal microfilariae recovered from specimens obtained from umbilical and cervical sites of cattle infected with adult Onchocerca gutturosa alone or with adults of O gutturosa and O lienalis were measured and compared with uterine microfilariae obtained directly from gravid female worms of each species. Uterine microfilariae of O gutturosa were longer than dermal microfilariae obtained from cattle harboring only adults of O gutturosa. Dermal microfilariae were recovered from umbilical and cervical sites in these cattle. Those found at the cervical site had lengths equal to or greater than lengths of microfilariae recovered from the umbilical site. There was a significant (P less than 0.0001) shift in length across populations of microfilariae of O gutturosa from various sites in its bovine host, with a progressive decrease in length between microfilariae recovered from the worm's uterus, microfilariae from the cervical dermis, and microfilariae from the umbilical dermis, respectively. A similar direct comparison was not possible for microfilariae of O lienalis, because none of the cattle was infected with only adult worms of this species. In an indirect comparison, microfilariae of O lienalis were identified at the umbilicus, but their presence in the cervical region could not be determined unequivocally because of confounding of microfilariae length by concurrent infection with O gutturosa. Uterine microfilariae from O lienalis were longer than uterine microfilariae of O gutturosa, although a degree of overlap in the range of measurements existed between species.

Algorithms↗
PubMed1979

Brugia malayi microfilaraemia in mice: a model for the study of the host response to microfilariae.

Microfilariae of Brugia malayi were obtained from the peritoneal cavities of infected gerbils and were then injected intravenously into mice. A sub-periodic, nocturnal microfilaraemia was produced. The level of microfilaraemia was proportional to the number of parasites injected, with approximately 1-3% of microfilariae being found in the peripheral circulation. The duration of microfilaraemia was proportional to the number of parasites injected; it subsided by 30 days after injection of 104 microfilariae but was still present at a low level 120 days after injection of 2 x 105 microfilariae. A transient splenomegaly developed after injection of microfilariae. Histopathological examination revealed large numbers of microfilariae free in the lumens of pulmonary small blood vessels and without any accompanying inflammatory reaction. Lesser numbers of microfilariae were seen in the cardiac blood and hepatic and renal blood vessels for the first few days after injection. There was cellular proliferation in the splenic white pulp and vascular congestion of the red pulp. Microfilariae labelled with 51Cr were injected intravenously; 57% of radioactivity was found in the lungs, 8.5% in the liver and 2.9% in the spleen. Mice developed immediate hypersensitivity reactions to B. malayi antigen by 4 weeks after injection, but Arthus and delayed hypersensitivity reactions were not seen at any time. when mice which had been injected 5 months previously were challenged with a 2nd injection of microfilariae, there was an accelerated clearance of parasites over 2 weeks and a marked peripheral blood eosinophilia developed. In contrast with natural infections, in which the continuous production of microfilariae complicates assessment, this model provides a system in which factors controlling the circulation of microfilariae in the bloodstream can be studied independently.

Animals↗
PubMed1975

Factors influencing the passage of Onchocerca volvulus microfilariae into the urine.

The effect of various substances on the output of Onchocerca volvulus microfilariae in the urine was investigated in volunteers infected with the Cameroon forest and Sudan-savanna strains of the parasite. Output of microfilariae in the urine tended to be higher during periods of normal activity than during sleep. During waking hours, the rate of output remained generally steady, but in some patients occasional showers of microfilariae appeared in the urine, possibly associated with the intake of food and drink. Drinking 1.2-2.5 litres water produced a shower of microfilariae in the urine of some subjects. This began within an hour of drinking and its onset preceeded that of the diuresis. Thiazide diuretics, acting on the convoluted tubules, produced no increase in microfilaruria. In savanna subjects intravenous injection of DT TAB vaccine caused pyrexia, and simultaneously large numbers of microfilariae appeared in the urine. There was no associated diuresis, and no increase in the concentration of microfilariae in the venous blood. In forest subjects DT TAB caused no increase in microfilaruria. In all subjects 25-50 mg diethylcarbamazine (DEC) caused large numbers of microfilariae to appear in the urine on day 0, within a few hours of the first dose; and there was an increased output of urine over the first 24 hours. Microfilaruria declined sharply on day 1 of treatment, but in subjects developing a high microfilaraemia, it rose again on day 2, and declined more slowly thereafter. Betamethazone, given in conjunction with DEC, appeared to slow the rate of destruction of microfilariae in the skin and lymph glands, and to prolong the duration of microfilaraemia and microfilaruria. The findings suggest that there is a reservoir of microfilariae in the glomerular capillaries, which fills slowly by accumulating microfilariae from the circulating blood. The microfilariae probably enter the urine by penetrating the glomerular capillary.

Adult↗
PubMed1979

Studies on Dipetalonema viteae (Filarioidea) 3. Antibody-dependent cell-mediated destruction of microfilariae in vivo.

Antibody-dependent cell-mediated destruction of Dipetalonema viteae microfilariae could be demonstrated in the golden hamster using a micropore chamber technique. Microfilariae were eliminated within 24 hours in chambers of 3.0 and 5.0 microm pore size when implanted into amicrofilaremic hamsters (week 30 post infection). At peak microfilaremia (week 12 post infection), only some hamsters could efficiently destroy microfilariae. In chambers with 0.3 microm pore size, microfilariae survived for more than 3 weeks in all hamsters. In uninfected hamsters, microfilariae could only be eliminated if they had been preincubated with serum or its 19S fraction containing antibodies to the cuticle of microfilariae. The opsonizing activity of the serum was abolished by 2-mercaptoethanol treatment. The composition of cells adhering to microfilariae was always significantly different from the composition of cells which migrated into a chamber. The adhesion patterns on individual microfilariae indicated that no single effector cell type was responsible for the destruction of microfilariae. The eosinophil was the predominant cell type but neutrophils, lymphocytes and monocytes also adhered to the microfilariae. Cellular adhesion led to the immobilization of microfilariae and subsequently to their disintegration within large cell clusters. During the final stages of destruction the contribution of the monocyte became more pronounced.

Animals↗
PubMed1979

The exsheathment of Brugia pahangi microfilariae under controlled conditions in vitro.

Two reproducible techniques for the exsheathment in vitro of microfilariae of Brugia pahangi, and other sheathed microfilariae, are described. Microfilariae were isolated from infected cat blood by filtration and suspended in Hank's Balanced Salt Solution. The first technique involved the incubation of isolated microfilariae for one hour in 20 mM CaCl2 in a phosphate-free Balanced Salt Solution, during which time approximately 90% of the microfilariae lost their sheaths. The second method of exsheathing microfilariae of B. pahangi involved exposure of microfilariae to solutions of endopeptidase (5.8 units/ml) or papaya extract protease (3.0 units/ml) in Ca2+-free HBSS. Exsheathment rates of 95--100% occurred within 30 minutes in both enzyme solutions. Both the Ca2+ ion and the endopeptidase technique have proven equally effective in stimulating exsheathment of microfilariae of Brugia malayi, Wuchereria bancrofti and Litomosoides carinii. Such artificially exsheathed microfilariae are used for in vitro cultivation studies. The viability of Ca2+- and endopeptidase-exsheathed microfilariae of B. pahangi has been confirmed by inoculation of exsheathed larvae into susceptible female mosquitoes.

Aedes↗
PubMed1976

Onchocercal dermatitis: ultrastructural studies of microfilariae and host tissues, before and after treatment with diethylcarbamazine (Hetrazan).

Specimens of skin from four Cameroon patients with severe onchocercal dermatitis, before and after treatment with diethylcarbamazine (DEC), were studied by light and electron microscopy. Microfilariae of Onchocerca volvulus have ultrastructural features resembling those of microfilariae of other genera. Between the surface layer of the cuticle and the trilaminate membrane, there is an electrolucent zone which is much wider in degenerating microfilariae than in intact microfilariae. Widening of the zone may result from DEC-induced release of component(s) of the cuticle, possibly collagen or mucopolysaccharide. Between the cuticle and dermal collagen there are granular deposits which might be immune complexes involving the collagenous component of cuticle. Others have shown that DEC does not kill microfilariae in vitro. Treatment with DEC presumably "unmasks" microfilariae in the skin so that they are recognized as foreign bodies and are destroyed by the host's defenses. Histiocytes and eosinophils are seen in close proximity to degenerating microfilariae. Enzymes from histiocytes and eosinophils might readily penetrate the cuticle altered by DEC treatment, and digest various components within the microfilariae. Alternatively, the widening of the electrolucent zone might result directly from the action of leucocytic or histiocytic enzymes, after the microfilaria has been killed by other mechanisms.

Adult↗
PubMed1987

Lectin-binding characteristics of Wuchereria bancrofti microfilariae.

The binding of 10 different lectins to the surface of microfilariae of Wuchereria bancrofti has been investigated. Wheat germ agglutinin (WGA) and Helix pomatia lectin (HPA) bound specifically to the sheathed microfilariae indicating the presence of N-acetyl-D-glucosamine and N-acetyl-D-galactosamine respectively on the surface. Exsheathed microfilariae did not react with any of the lectins. Treatment of sheathed microfilariae with proteases resulted in increased binding of WGA and HPA. Such treated microfilariae showed a weak binding of Concanavalin A (Con A), and lectins of lentil (LCH) and of Limulus polyphemus (LPA). Sheathed microfilariae incubated with sera of people living in endemic zones of filariasis but with no apparent evidence of infection (endemic normals), or with sera of chronic elephantiasis patients, or with their respective gamma globulin fractions, bound Con A and LCH. These lectins bound weakly to exsheathed microfilariae under the same conditions. Binding was due to the mannose components of the specific immunoglobulins of the sera which coated the microfilariae. However, microfilariae when incubated with sera or their globulin fractions from non-endemic normals (NEN), or from microfilarial carriers, did not bind Con A and LCH, suggesting that specific immunoglobulins were neither present in NEN sera nor in significant amounts in sera of microfilarial carriers.

Acetylgalactosamine↗
PubMed1990

Distribution of microfilariae of Onchocerca lienalis and Onchocerca gutturosa in the skin of cattle in Germany and their development in Simulium ornatum and Culicoides nubeculosus following artificial infestation.

Onchocerca microfilariae were isolated form the umbilicus and neck of 438 cow hides at the abattoir in Tübingen, F.R.G. The overall Onchocerca infection rate was 40.4%. The presence of Onchocerca lienalis and O. gutturosa microfilariae, which are difficult to distinguish by morphological criteria, was retrospectively demonstrated after artifically infesting Simulium ornatum and Culicoides nubeculosus and identifying the infective larvae recovered. Nine of 16 samples of umbilical microfilariae fed to C. nubeculosus through a latex membrane developed to O. gutturosa third stage larvae (L3). Six of seven umbilical samples injected into the thorax of S. ornatum yielded O. lienalis L3. In six infestation trials in which microfilariae were introduced both into S. ornatum and C. nubeculosus, O. lienalis L3 were recovered exclusively from simuliids, while O. gutturosa L3 developed only in midges. Of six umbilical skins tested by cross-infestation, one contained exclusively O. gutturosa microfilariae, four only O. lienalis microfilariae and one was infected with both species. Developmental success of O. lienalis microfilariae to L3 in S. ornatum following intrathoracic injection was 22% of the mean inoculum. O. gutturosa microfilariae, ingested by C. nubeculosus through a latex membrane, developed to L3 at a rate of 2.3% of the mean microfilarial uptake.

Animals↗
PubMed1992

Brugia malayi: ivermectin inhibits the exsheathment of microfilariae.

Brugia malayi-infected microfilaremic jirds (Meriones unguiculatus) were treated with ivermectin at a single dose of 200 micrograms/kg of body weight injected subcutaneously. Susceptible Aedes aegypti mosquitoes were fed on treated jirds 24 hours later. Mosquitoes fed on untreated jirds served as controls. Infected mosquitoes were dissected at 1, 3, 24, 48, 72, and 96 hr after the blood meal, and differential counts of sheathed microfilariae, exsheathed microfilariae, and cast sheaths were performed using fluoresceinated wheat germ agglutinin. Microfilariae failed to exsheath in mosquitoes fed on ivermectin-treated jirds. Microfilariae from ivermectin-treated jirds also did not exsheath in vitro in the presence of 10 mM CaCl2, whereas 85-90% of sheathed microfilariae from untreated jirds exsheathed in vitro. In addition, sheathed microfilariae from untreated jirds, when pretreated in vitro with ivermectin at 0.25, 0.5, or 1 microgram/ml, lost their ability to exsheath in vitro in the presence of 10 mM CaCl2. However, ivermectin treatment had no effect on exsheathing of microfilariae when incubated with papaya protease. Thus, ivermectin appears to inhibit the intrinsic exsheathing process of microfilariae in the mosquito host, thereby blocking their development and further transmission of infection.

Aedes↗
PubMed1988

Biochemical and immunochemical characterization of surface and excretory-secretory antigens of Loa loa microfilariae.

Detergent solubilized extracts of 125Iodogen surface-labelled Loa loa microfilariae revealed a relatively simple profile of two strongly labelled molecules of 23 and 67 kDa for blood microfilariae and several strongly labelled molecules of 23, 40, 42-67 kDa for in vitro born microfilariae. In addition, there were other weakly labelled molecules which were resolved after prolonged autoradiographic exposure. Surface molecules of 28, 29, and 33 kDa were unique to blood microfilariae, a 14.4 kDa molecule was unique to in vitro born microfilariae and molecules of 23, 40, and 75-84 kDa were common to both forms of microfilariae. The profile of excretory-secretory products consisted of molecules of 14.4-198 kDa. Human albumin was a predominant component of surface molecules and excretory-secretory products from blood microfilariae. Immunoprecipitation with occult and microfilaremic loaiasis sera demonstrated that the 23 kDa surface molecule and excretory-secretory products of 14.4 and 33 kDa were only recognized by occult loaiasis sera whereas surface molecules of 40 and 75-84 kDa and excretory-secretory products of 28 and 67 kDa were recognised by both sera. Studies with heterologous sera demonstrated that with the exception of the 75-84 kDa antigens, all the L. loa microfilarial surface antigens contained epitopes which were restricted to filarial parasites. Further studies revealed that the 23 kDa antigen was a protein which contained neither asparagine-N-linked oligosaccharides nor interchain disulfide-linkages.

Animals↗
PubMed1989

The relationship between microfilarial density and uptake of Foleyella candezi microfilariae by Aedes aegypti.

There was a linear regression in the square root of the numbers of microfilariae abstracted (square root of y) by Aedes aegypti refm strain on the square root of the density of microfilariae in the infecting blood (square root of x). The linear regression is represented by the equation, square root of y = 0.080,59 square root of x + 4.556 (r = 0.627; P less than 0.01). - Ae. aegypti abstracted microfilariae about 1.60 times that expected from the infecting blood meal. This value however decreased, when the microfilariae in the infecting blood meal increased possibly due to error in counting large numbers of microfilariae. - The volumes of blood ingested by three strains of Aedes aegypti (+fm/+fm, refm/refm, reF/reF) appeared to be unaffected by genes controlling susceptibility or refractoriness to filariae (Foleyella candezi). - The Duncan's multiple range test showed similarity (p greater than 0.01) in percentage uptake efficiency, 157.28 and 164.28 for black-eyed homozygous susceptible and red-eyed homozygous susceptible strains respectively. There was significant difference between either of the homozygous susceptible strains and the homozygous refractory triple marker strain (calculated F-value = 28.61; critical tabular F-value = 10.92; p less than 0.01). Therefore, the % uptake efficiency of Ae. aegypti for F. candezi microfilariae is influenced by the gene (fm) which also allows the development of the filariae. - The percentage efficiency (observed/expected X 100) in abstracting microfilariae from infecting blood source by homozygous susceptible strains was about twice that (80.98%) observed for a homozygous refractory triple marker strain.

Aedes↗
PubMed1991

Experimental ocular onchocerciasis in cynomolgus monkeys. IV. Chorioretinitis elicited by Onchocerca volvulus microfilariae.

Onchocerciasis is a major cause of blindness worldwide, and much of the blindness is caused by onchocercal chorioretinitis. In an experimental animal model for ocular onchocerciasis, intravitreal injections of 10,000 live Onchocerca volvulus microfilariae isolated from infected humans into the eyes of cynomolgus monkeys (Macaca fascicularis) resulted in patchy, progressive loss of retinal pigment with pigment clumping. Areas of pigment loss were less extensive in animals that had been sensitized with microfilariae. Intravitreal injections of dead O. volvulus microfilariae resulted in mild vitritis with relatively less clinical change noted in the retina and choroid. Histopathologic examination revealed thinning and loss of outer retinal layers with pigment migration into the retina, and inflammation was more pronounced in eyes that received live microfilariae. Clinical changes appeared in eyes receiving live microfilariae before the development of significant antibody or cell-mediated immune responses. O. volvulus microfilariae appear to be more suitable than O. lienalis microfilariae in producing lesions which resemble human onchocerciasis in the primate model.

Animals↗