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Morphogenesis of developmental stages of Dirofilaria immitis (Nematoda) in the dog
... L3 injected into diffusion chambers are too large to escape through the membrane pores yet host cells and humoral factors can freely enter. D. immitis L3 inserted into diffusion chambers and then implanted subcutaneously into mice or dogs were shown to survive and grow at equal rates for at least three weeks, although the rates of development were reduced from that described in tissues of dogs 8,11 . NOD.Cg-Prkdc scid Il2rg tm1Wjl /SzJ (NSG) mice have profound defects in both innate and adaptive and immune responses 12 including: (1) loss of both T and B cell function 13 , (2) macrophages, NK cells and dendritic cells are found in NSG mice but are functionally compromised, (3) defects in the complement cascade 14,15 , (4) eosinophils are found in the bone marrow of NSG mice but not in the peripheral blood 16 and (5) monocytes and neutrophils are present in NSG mice although their functional capacity is unknown 15 . ...
... Analysis of the lengths of the recovered worms suggested that the parasite growth rate was linear in the NSG mice over the 15 week infection period with R 2 coefficient of determination = 0.9797. For the purposes of comparison, the lengths of D. immitis recovered from dogs at different time points from two previous studies (Orihel 9 and Lichtenfels et al. 8 were added to Fig. 1). During the first 30-35 days of infection, worms recovered from NSG mice and from dogs apparently develop at the same rate achieving equivalent lengths. ...
... This was possible based on the length of the life cycle and the size of the worms. This was not possible for O. volvulus infections of NSG mice, in which, like D. immitis, development appears to be limited to development from L3 to The description of D. immitis larval development from the L3 to the adult worm in the dog, the natural definitive host, has been well documented 8,9 . This report does not attempt to redescribe that development. ...
Heartworm disease, caused by Dirofilaria immitis, remains a significant threat to canines and felines. The development of parasites resistant to macrocyclic lactones (ML) has created a significant challenge to the control of the infection. The goal of this study was to determine if mice lacking a functional immune response would be susceptible to D. immitis . Immunodeficient NSG mice were susceptible to the infection , sustaining parasites for at least 15 weeks, with infective third-stage larvae molting and developing into the late fourth-stage larvae. Proteomic analysis of host responses to the infection revealed a complex pattern of changes after infection, with at least some of the responses directed at reducing immune control mechanisms that remain in NSG mice. NSG mice were infected with isolates of D. immitis that were either susceptible or resistant to MLs, as a population. The susceptible isolate was killed by ivermectin whereas the resistant isolate had improved survivability, while both isolates were affected by moxidectin. It was concluded that D. immitis survives in NSG mice for at least 15 weeks. NSG mice provide an ideal model for monitoring host responses to the infection and for testing parasites in vivo for susceptibility to direct chemotherapeutic activity of new agents.
... In experimental infections, most larvae are recoverable in the vicinity of the inoculation site 3 to 7 days later, suggesting little initial migration [11,12]. The molt from L3 to L4 occurs 2 to 5 days post-infection, with the final molt occurring 50 to 70 days post-infection [13][14][15][16]. Aberrant arrival of filarial larvae in the pulmonary alveoli is followed by their immunemediated death, so D. immitis avoids the cardiopulmonary system until attaining a suitable size (20-40 mm in length) at day 70-85 post-infection [16][17][18]. ...
... When cultured separately, almost all D. immitis L3 demonstrated attachment by one or more jird-derived PECs when examined at 20 h (mean = 99.6%), while B. malayi demonstrated very low levels of attachment (mean = 5.3%); this difference was significant (U (14,15) = 0, p < 0.001; Fig. 1). Similar results were observed when both species were co-cultured, with no significant change in cell attachment to D. immitis in the presence of B. malayi (U (9,14) = 58.5, p = 0.999). ...
... Nonetheless, attachment rates between heatkilled worms of each species remained significantly different (U (11,9) = 0, p < 0.001). In culture conditions where PECs were derived from jirds bearing mature B. malayi infection, we observed similar results as with filarianaïve jirds (mean = 99.4% and 4.72% of D. immitis and B. malayi, respectively), with no significant change in attachment to D. immitis (U (12,14) = 68.5, p = 0.255) or B. malayi (U (12,15) = 80, p = 0.621). A high degree of variability in the number of cells attaching to D. immitis L3 was noted, from a single cell to a number that covered approximately 90% of the length of the larva; the number of cells attaching to B. malayi L3, however, were always very few, covering no more than approximately 10% of the length of the worm. ...
Background
The Mongolian jird ( Meriones unguiculatus ) has long been recognized as a permissive host for the filarial parasite Brugia malayi ; however, it is nonpermissive to another filarial parasite, canine heartworm ( Dirofilaria immitis ). By elucidating differences in the early response to infection, we sought to identify mechanisms involved in the species-specific clearance of these parasites. We hypothesized that the early clearance of D. immitis in intraperitoneal infection of the jird is immune mediated and parasite species dependent.
Methods
Jird peritoneal exudate cells (PECs) were isolated and their attachment to parasite larvae assessed in vitro under various conditions: D. immitis and B. malayi cultured separately, co-culture of both parasites, incubation before addition of cells, culture of heat-killed parasites, and culture with PECs isolated from jirds with mature B. malayi infection. The cells attaching to larvae were identified by immunohistochemistry.
Results
In vitro cell attachment to live D. immitis was high (mean = 99.6%) while much lower for B. malayi (mean = 5.56%). This species-specific attachment was also observed when both filarial species were co-cultured, with no significant change from controls ( U (9, 14) = 58.5, p = 0.999). When we replicated these experiments with PECs derived from jirds subcutaneously infected with B. malayi , the results were similar (99.4% and 4.72% of D. immitis and B. malayi , respectively, exhibited cell attachment). Heat-killing the parasites significantly reduced cell attachment to D. immitis (mean = 71.9%; U (11, 14) = 7.5, p < 0.001) while increasing attachment to B. malayi (mean = 16.7%; U (9, 15) = 20, p = 0.002). Cell attachment to both species was reduced when larvae were allowed a 24-h pre-incubation period prior to the addition of cells. The attaching cells were identified as macrophages by immunohistochemistry.
Conclusions
These results suggest a strongly species-dependent response from which B. malayi could not confer protection by proxy in co-culture. The changes in cell attachment following heat-killing and pre-incubation suggest a role for excretory/secretory products in host immune evasion and/or antigenicity. The nature of this attachment is the subject of ongoing study and may provide insight into filarial host specificity.
... In the mosquito, the microfilariae moult before migrating to the proboscis as D. immitis infective third-stage larvae (L3) [9]. These larvae (L3) are transferred to hosts during blood meals, where migrate throughout the blood and body towards the pulmonary arteries and reach sexual maturity in large blood vessels [10]. The microfilariae are first seen in 6-7 month after the initial infection and the life span of adult female (230-310 mm in length) and male (120-190 mm in length) heartworms is 5-10 years [8][9][10]. ...
... These larvae (L3) are transferred to hosts during blood meals, where migrate throughout the blood and body towards the pulmonary arteries and reach sexual maturity in large blood vessels [10]. The microfilariae are first seen in 6-7 month after the initial infection and the life span of adult female (230-310 mm in length) and male (120-190 mm in length) heartworms is 5-10 years [8][9][10]. ...
Background
Heartworm (Dirofilaria immitis) in dogs is considered endemic in Australia, but the clinical heartworm disease caused by the heartworm is rare and prevalence is low. The mainstream prevention of the heartworm is based on macrocyclic lactone (ML) administration. The aim of this study was to confirm endemism of the heartworm under current Australian conditions using a cohort of recent microfilaria-positive dogs which were on variable heartworm prevention. MethodsA hotspot of canine heartworm antigen-positive and microfilaria-positive dogs has been detected recently in Queensland, Australia. Blood samples from 39 dogs from Queensland and two dogs from New South Wales were investigated for canine filarioids. Rapid antigen diagnostic tests capable of detection of D. immitis and real-time PCR for quantification and differentiation between D. immitis from Acanthocheilonema reconditum with quantification of microfilariae in canine blood samples, together with D. immitis specific real-time PCR assay, were applied to microfilaria-positive dogs. The P-glycoprotein genotype was determined to test whether Australian-sourced heartworm shared the same genetic markers as those suspected of ML-resistance in North America. ResultsOnly D. immitis was detected in the samples from Queensland and New South Wales, Australia. Using high resolution melt real-time PCR and D. immitis specific real-time PCR, the calculated microfilaria concentration ranged from 1 to 44,957 microfilariae/ml and from 7 to 60,526 microfilariae/ml, respectively. DNA sequencing of the PCR products confirmed D. immitis. Fifteen of the examined dogs were on putative, rigorous ML prevention. For the remaining dogs, compliance with heartworm prevention was unknown or reported as inconsistent. Wild-type genotype AA-GG of the P-glycoprotein locus of D. immitis sequence has been obtained for three blood samples. Due to the incomplete history, any suggestion of a loss of efficacy of MLs must be treated as ‘remotely possible’. In the immediate future, records of preventative administration and annual antigen testing would be required to determine any problems with the efficacy of preventatives. Conclusions
The prevalence of canine heartworm in Australia remains poorly understood. It is generally assumed to be low by veterinary practitioners. The localised increase in the study area confirms endemism of canine heartworm and a requirement for ongoing vigilance through annual heartworm testing to better understand the changing distribution of canine heartworm, client compliance, as well as to detect any change in ML-susceptibility.
... Microfilaria must go through two development stages within a mosquito before being deposited close to the vector feeding site on the host's skin (Knight and Lok, 1998). They then migrate into the skin puncture and undergo maturation and moults in the host muscle tissues (Lichtenfels et al., 1985), finally maturing and living in the pulmonary vasculature, a process that takes at least six months (McCall et al., 2008;Bowman and Atkins, 2009). Heartworms originate exclusively exogenously from mosquito-based transmission and cannot replicate endogenously (i.e. ...
Canine heartworm, Dirofilaria immitis, can cause severe disease and sometimes death of the host. Associated clinical signs, lack of preventative usage and regional endemicity are unlikely sufficient by themselves to reach a definitive diagnosis. Several point-of-care (POC) diagnostic tests are commercially available to aid in-clinic diagnosis, however, there is variable diagnostic accuracy reported and no synthesis of published evidence. This systematic review aims at meta-analysing the likelihood ratio of a positive result (LR+) to inform the selection and interpretation of POC tests in practice to rule-in heartworm infection when there is clinical suspicion. Three literature index interfaces (Web of Science, PubMed, Scopus) were searched on November 11th, 2022, for diagnostic test evaluation (DTE) articles assessing at least one currently commercialised POC test. Risk of bias was assessed adapting the QUADAS-2 protocol and articles with no evidence of high risk of bias were meta-analysed if deemed applicable to our review objective. Substantial between DTE heterogeneity was investigated including potential threshold or covariate effects. A total of 324 primary articles were sourced and 18 were retained for full text review of which only three had low risk of bias in all four QUADAS-2 domains. Of the nine heartworm POC tests evaluated, only three, IDEXX SNAP (n DTEs = 6), Zoetis WITNESS (n DTEs = 3) and Zoetis VETSCAN (n DTEs = 5) could be analysed. Both WITNESS and VETSCAN DTEs showed substantial heterogeneity due to a putative threshold effect and no summary point estimates could be reported. SNAP DTEs showed acceptable heterogeneity, and a summary LR+ was estimated at 559.0 (95%CI: 24.3-12,847.4). The quality and heterogeneity of heartworm POC test DTEs was highly variable which restricted our summary of the diagnostic accuracy to only the SNAP test. A positive result from the SNAP test provides strong evidence of the presence of an infection with adult heartworm(s) in a dog patient and this test is warranted to rule-in clinical suspicion(s) in clinics. However, our review did not appraise the literature to assess the fitness of SNAP test, or any other POC tests, to rule-out heartworm infection in dogs without clinical suspicion or following heartworm therapy.
... However, anterior morphogenesis was partially arrested in vitro compared with NSG mouse-derived larvae ( Figure 2C). In the dog, larvae complete the L3-L4 molt rapidly, the vast majority by 3 days post-infection (Lichtenfels et al., 1985). In our cultures, ∼50% of the day 14 L4 had completed molting, with cuticle casts evident in the culture media. ...
Introduction
Dirofilariasis, including heartworm disease, is a major emergent veterinary parasitic infection and a human zoonosis. Currently, experimental infections of cats and dogs are used in veterinary heartworm preclinical drug research.
Methods
As a refined alternative in vivo heartworm preventative drug screen, we assessed lymphopenic mouse strains with ablation of the interleukin-2/7 common gamma chain (γc) as susceptible to the larval development phase of Dirofilaria immitis.
Results
Non-obese diabetic (NOD) severe combined immunodeficiency (SCID)γc−/− (NSG and NXG) and recombination-activating gene (RAG)2−/−γc−/− mouse strains yielded viable D. immitis larvae at 2–4 weeks post-infection, including the use of different batches of D. immitis infectious larvae, different D. immitis isolates, and at different laboratories. Mice did not display any clinical signs associated with infection for up to 4 weeks. Developing larvae were found in subcutaneous and muscle fascia tissues, which is the natural site of this stage of heartworm in dogs. Compared with in vitro-propagated larvae at day 14, in vivo-derived larvae had completed the L4 molt, were significantly larger, and contained expanded Wolbachia endobacteria titres. We established an ex vivo L4 paralytic screening system whereby assays with moxidectin or levamisole highlighted discrepancies in relative drug sensitivities in comparison with in vitro-reared L4 D. immitis. We demonstrated effective depletion of Wolbachia by 70%−90% in D. immitis L4 following 2- to 7-day oral in vivo exposures of NSG- or NXG-infected mice with doxycycline or the rapid-acting investigational drug, AWZ1066S. We validated NSG and NXG D. immitis mouse models as a filaricide screen by in vivo treatments with single injections of moxidectin, which mediated a 60%−88% reduction in L4 larvae at 14–28 days.
Discussion
Future adoption of these mouse models will benefit end-user laboratories conducting research and development of novel heartworm preventatives via increased access, rapid turnaround, and reduced costs and may simultaneously decrease the need for experimental cat or dog use.
... To collect D. immitis excretory/secretory crude antigen (ES antigen) free of antibody, live heartworms recovered as part of previous studies were used [9]. Altogether, nine sets of recovered mature heartworms consisting of three groups of two males each, three groups of two females each and three groups of two males/two females each were briefly rinsed in warm tap water to lyse and remove blood clots and visually assessed to determine sex, viability and length measured to confirm maturity [20,21]. The nine groups of mature heartworms were briefly transferred to individual sterile 50-ml centrifuge tubes containing 40 ml sterile water and gently inverted three times. ...
Background:
Immune complexing of target antigen to high affinity host antibody is recognized to impact the sensitivity of commercial heartworm antigen tests. Published information describing the effect of heat on interfering canine host antibodies is lacking. Immune complex dissociation (ICD) by heat treatment of serum for samples initially testing negative for heartworm antigen increases sensitivity of commercial antigen tests, particularly for single sex or low adult infection intensities. In this study the stability and nature of the targeted epitope and mechanism of heat ICD were examined.
Methods:
Canine IgG was isolated using protein-A columns from serum originating from four dogs evaluated after necropsy: one dog with evidence of previously cleared infection and three dogs with confirmed heartworm infections. These dogs were expected to have an excess of antibodies based on negative antigen test and to have no or low antigen optical density, respectively, following heat treatment. Interference of antigen detection on (non-heated) positive serum was evaluated, following 1:1 mixing of antibody/PBS solutions previously heated at 25 °C, 65 °C, 75 °C, 85 °C, 95 °C and 104 °C, compared to positive serum/PBS control measured by optical density using a commercial heartworm antigen ELISA and protein quantification. Live heartworms incubated in media for 72 h provided excretory/secretory antigen for antigen stability studies following heat, endopeptidase digestion and disulfide bond reduction.
Results:
Mixing antigen-positive heartworm serum with antibody solutions demonstrated a significant inhibition of antigen detection for antibody solutions previously heated at 25 °C and 65 °C relative to positive serum/PBS control. Antigen detection optical density was restored at or above the control when positive serum was mixed with solutions previously heated at 75 °C, 85 °C, 95 °C and 104 °C. Significant changes occurred in protein levels for antibody solutions heated at 75 °C, 85 °C, 95 °C and 104 °C. Relative stability of antigen from live heartworms in culture was demonstrated following heat, chemical and enzymatic treatment.
Conclusions:
Significant changes in protein levels and antigen binding ability occurred in IgG solutions heated above 65 °C. The findings confirm heat denaturation of antibodies as the suspected mechanism of heat ICD at 104 °C for antigen diagnosis of heartworm. No significant change occurred in antigen detection following heat, chemical or enzymatic digestions supporting a heat-stable linear nature of the epitope.
... Apparently, L3 and L4 travel between muscle fibres during migration, whereas juveniles (immature adults) penetrate muscle and eventually the jugular, or other veins, directing them towards the heart (Kotani and Powers, 1982;Kume and Itagaki, 1955;Orihel, 1961). The molt from L3 to L4 begins as early as day 3 (Kotani and Powers, 1982;Lichtenfels et al., 1985) and as late as day 9-12 (Orihel, 1961). L4 molt to the final stage at day 50-70; the first worms entering the heart on day 70-85 are 2-4 cm in length. ...
Heartworm disease due to Dirofilaria immitis continues to cause severe disease and even death in dogs and other animals in many parts of the world, even though safe, highly effective and convenient preventatives have been available for the past two decades. Moreover, the parasite and vector mosquitoes continue to spread into areas where they have not been reported previously. Heartworm societies have been established in the USA and Japan and the First European Dirofilaria Days (FEDD) Conference was held in Zagreb, Croatia, in February of 2007. These organizations promote awareness, encourage research and provide updated guidelines for the diagnosis, treatment and prevention of heartworm disease. The chapter begins with a review of the biology and life cycle of the parasite. It continues with the prevalence and distribution of the disease in domestic and wild animals, with emphasis on more recent data on the spreading of the disease and the use of molecular biology techniques in vector studies. The section on pathogenesis and immunology also includes a discussion of the current knowledge of the potential role of the Wolbachia endosymbiont in inflammatory and immune responses to D. immitis infection, diagnostic use of specific immune responses to the bacteria, immunomodulatory activity and antibiotic treatment of infected animals. Canine, feline and ferret heartworm disease are updated with regard to the clinical presentation, diagnosis, prevention, therapy and management of the disease, with special emphasis on the recently described Heartworm Associated Respiratory Disease (HARD) Syndrome in cats. The section devoted to heartworm infection in humans also includes notes on other epizootic filariae, particularly D. repens in humans in Europe. The chapter concludes with a discussion on emerging strategies in heartworm treatment and control, highlighting the potential role of tetracycline antibiotics in adulticidal therapy.
A 6-year-old neutered female cat was examined for chronic and progressive pelvic limb ataxia that progressed to non-ambulatory paraparesis over 1 month. Haematological and serum analyses were mainly within normal ranges. Thoracic and abdominal radiographs did not reveal any morphological abnormalities. Magnetic resonance imaging investigation of the thoraco-lumbar spine demonstrated a well-defined, extradural mass that extended into the epidural space from the L2 to L3 vertebral bodies and expanded in the L2 to L3 left intervertebral foramen. During surgery, a long, narrow, white parasite that was weakly adherent to the phlogistic epidural fat tissue was gently removed from the spinal canal. Histological examination of the pathological tissue supported a diagnosis of epidural steatitis surrounding a female adult Dirofilaria immitis. This is a novel case of natural D immitis infection with spinal localisation in a cat, well documented with magnetic resonance investigation, and cytological and histological examinations, introducing a novel differential diagnosis for extradural spinal masses in cats.
Dirofilariasis represents a zoonotic mosaic, which includes two main filarial species (Dirofilaria immitis and D. repens) that have adapted to canine, feline, and human hosts with distinct biological and clinical implications. At the same time, both D. immitis and D. repens are themselves hosts to symbiotic bacteria of the genus Wolbachia, the study of which has resulted in a profound shift in the understanding of filarial biology, the mechanisms of the pathologies that they produce in their hosts, and issues related to dirofilariasis treatment. Moreover, because dirofilariasis is a vector-borne transmitted disease, their distribution and infection rates have undergone significant modifications influenced by global climate change. Despite advances in our knowledge of D. immitis and D. repens and the pathologies that they inflict on different hosts, there are still many unknown aspects of dirofilariasis. This review is focused on human and animal dirofilariasis, including the basic morphology, biology, protein composition, and metabolism of Dirofilaria species; the climate and human behavioral factors that influence distribution dynamics; the disease pathology; the host-parasite relationship; the mechanisms involved in parasite survival; the immune response and pathogenesis; and the clinical management of human and animal infections.
This article is a review of the systematics, taxonomy, biology, prevention, control, and treatment of the canine heartworm, Dirofilaria immitus. This filarioid parasite remains one of the most important and dangerous diseases of the dog throughout the United States. The geographic range of the parasite is expanding, and in many parts of the country it has emerged as a threat to canine welfare only in the last 50 or so years. The article also discusses the pathophysiological mechanisms behind the disease induced, the means for diagnosing the disease, and the means of assessing the success of therapy. The treatment of potential complications of heartworm infection, such as post-adulticide thromboembolism, eosinophilic granulomatous pneumonitis, and caval syndrome, is also discussed.
Transmission electron microscopic investigation of the morphogenesis of Onchocerca volvulus through the third moult to the post-infective stage revealed essential alterations in various larval organs. Complete rebuilding of surface structures, the reduction of secretory granules in the glandular oesophagus, the unfolding of the intestine, an increase in the number of nerve fibres in the nerve ring and novel sensory papillae were significant findings. Transition from third- to fourth-stage larvae (L4) started as early as 48 h after transfer to vertebrate conditions in vivo in surrogate hosts and in vitro. After a resting period of about 60 h to enable a reduction in gland size and the loosening of the old cuticle and formation of the new one, the larvae started to cast the infective-stage cuticle. Young L4 exhibited a thin, monolayered cuticle and did not rebuild a glandular oesophagus. The body cavity widened, the intestine unfolded and the increased number of microvilli indicated the resumption of metabolic activity.
The electron microscopic investigation of the anterior part of the infective third-stage juvenile of Onchocerca volvulus provides first insights into the structure of the excretory system of this developmental stage of the parasite. The most anterior part of this system consists of a cell process of the syncytial excretory cells. At this height the excretory cells enclose the cuticle-lined excretory channel. The channel is in the process of elongation in the anterior-posterior direction, indicated by cell division in this region. More posteriad an ampulla-like structure is forming in the cytoplasm of the excretory cells. The inner surface of this ampulla is lined with a small number of single microvilli. In this part of the system the cytoplasm of the excretory cells is rich in Golgi bodies and endocytic vesicles. The ampulla has direct access to the exterior by the excretory duct. The excretory duct is a cuticle-lined structure surrounded by supporting fibres of an additional cell. This duct cell connects the excretory duct to the body-wall cuticle at the excretory pore. Adjacent to the region of the excretory system a cell is found that resembles a gland cell. This cell is in close contact to the ventral nerve cord. The genital primordia of the third-stage juvenile consist of several dividing cells. The female genital primordium is seen at the junction of the muscular with the glandular oesophagus and the male primordium can be found at the junction of the glandular oesophagus with the gut.
Microtopographic features of the various growth stages of the three free-living larval stages of the rat hookworm Nippostrongylus brasiliensis (Nematoda) were surveyed by scanning electron microscopy. These worms have a rounded anterior end and an elongated tail. Cuticular annulations were observed along the body, which also bore two ribbon-like lateral alae. Two rings of six lip-like lappets were observed around the triradiate oral opening in all larval stages. The cephalic space contained two lateral amphidial pits. The excretory pore in the third anterior part was observed in a ventral view of the larvae. No deirids were observed. The anus with a crescent-shape opening was located posteriorly. Phasmidial apertures, only observed in the third-stage larvae, opened on the lateral alae in the tail region.
An assessment was made of the capacity for re-migration of the 5th-stage juvenile canine heartworm, Dirofilaria immitis. Live, 5th-stage juvenile worms recovered from the pulmonary arteries of infected dogs were transplanted into the subcutaneous tissue of uninfected dogs, cats, and rabbits. A mean of 45%, 61%, and 18% of the transplanted worms were recovered from the pulmonary arteries of dogs, cats, and rabbits, respectively, 1 and 3 mo later. The 5th-stage juvenile worms thus have the ability to re-migrate through tissue into the pulmonary arteries of the host.
The development of the human filaria Loa loa (Dirofilariinae, Onchocercidae), previously studied in monkeys, was studied using the non permissive hosts-mice and jirds. The development proved to be rapid: moult 3 occurred on day 8 post-inoculation, the adult stage was reached on day 25 and measured at that time 3-3.5 mm in length. As in the other filarioids, the female genital apparatus developed during the fourth stage. A critical analysis of the studies on the development of Onchocercid species was made. The optimal duration of the stages (i.g. the shortest time) was chosen for the comparison. It appeared that the duration of the stage 3 was a constant character in a given species whatever the experimental conditions, whereas moult 4 might be retarded in a non susceptible host. Comparison between the 18 developmental cycles of Onchocercidae in the vertebrate host was made. Two biological types could be distinguished: either the moult 3 occurred on day 2-3 and was followed apparently by a late moult 4 (> or = 50 days), or the moult 3 occurred after about one week of development and it was associated with a less long stage 4 (20-40 days). The first group includes Dirofilaria and Onchocerca, the second group brings together mainly Loa and the Onchocercinae of the Dipetalonema line and related genera (Acanthocheilonema, Brugia, Litomosoides, etc.). The groups thus formed suggest real relationships as they fit with the morphology of the infective stage and the results of a recent molecular analysis of the 5S DNA.
Two prominent, asymmetrically placed cuticular somatic sensilla, called centrids, are reported in Ascaris suum Goeze, 1782, the pig roundworm. The right centrid is situated much more anteriorly on the body than is the left one. The centrids are globular in the fourth-stage larva and obviously void of an apical pore, suggesting at least a tactile function. In adult worms, the centrids are platelike, lacking a globular expansion. The observation on the presence of asymmetrically placed centrids in A. suum gives further impetus to the importance assigned to sense organs in the classification and identification of nematodes. The name centrid was originally chosen to indicate the placement of the papillae in the midbody region of worms. The name centrid, rather than, e.g. postdeirid, is proposed to be used when denoting asymmetrically oriented midbody sensilla among the Ascaridida and papillae, when shown homologous to these, of species within the Rhabditea generally. This proposal is in line with the name "Mittelkörperpapillen" originally adopted to denote homologous sensillae in Cucullanidae (Seuratoidea) by Törnquist in 1931.
This paper attempts to pinpoint the most original morphological anatomical features of the biology of filariae per se and those which are or could be important for triggering regulatory processes in the arthropod vector and uncontrolled pathogenic processes in the vertebrate hosts. The following stages are considered: the motile egg or newly-hatched larva, the microfilaria, in the lymphatic or blood vessels of its vertebrate host; the larva, its migrations and its intrasyncitial development in the hematophagous arthropod subverted as vector; its transfer to the vertebrate host, migratory properties through the lymphatic system, maturation, mating and, finally, egg laying in the tissues they reach. This synthesis is based on parasite morphological features and their functional interpretation, histological features in the different niches the filariae reach, and on quantitative analyses of filarial development at its different phases, as well as on the rare and valuable observations of living parasites in situ. Data have been drawn from various species of Onchocercidae from amphibians, reptiles, birds and mammals. These comparative analyses have revealed the major constraints to which the filariae, including those parasitizing humans, have been subjected during their evolution from their ancestors, the oviparous and heteroxenic spirurids. Emphasis is placed on mechanical events: resistance of the microfilariae to the currents in the blood or lymph vessels, regulatory processes induced in the vector mesenteron by the movements of the ingested microfilariae, transient disruption by the microfilarial cephalic hook of the vectors' tissues and cell membranes during microfilarial translocation, attachment of males to females during mating by means of 'non-slip' systems, etc. Like other nematodes, filariae are equipped with sensory organs and a locomotor system, composed of the muscles and of the original osmoregulatory-excretory cell. Any change in one of these elements will result in the destruction of the filaria, at some stage of its development. In the vertebrate host, the intravascular stages will no longer be able to resist being carried passively towards the organs of destruction such as the lymph nodes or the lungs.
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