The adherence in vitro of leucocytes to the surface of various stages in the life cycle of T. spiralis and N. brasiliensis in the presence of serum was examined. Considerable differences were observed in the behaviour of mast cells, eosinophils, neutrophils and macrophages in this interaction. Mast cells adhered for a short time, did not flatten onto the surface and did not degranulate. Adherence ceased after 4-6 hr. Eosinophils adhered within minutes to the surface or worms, flattened and degranulated; only their cytoplasmic remnants could be seen on the worms' surface after 24 hr in culture. In contrast, only a small area of the cytoplasmic membrane of neutrophils flattened on the surface of the worms and adherence ceased after 2-24 hr. The NBT conversion reaction showed a positive deposit at the interface between neutrophils and parasites during neutrophil adherence. This deposit remained as "foot prints" on the surface of the nematodes following neutrophil detachment. This positive NBT reaction occurred only with neutrophils and not with eosinophils, mast cells or macrophages. Macrophages adhered permanently to the surface of these worms, they did not flatten and retained their integrity. Under the light microscope the cytoplasmic inclusions appeared to decrease in size during culture. Electron microscopy revealed the presence of fewer granules and an increased number of vacuoles in later cultures of macrophages. These findings are discussed in relationship to the immunopathology of nematode infection in vivo.
This report describes the effect on various stages in the life cycle of the nematodes T. spiralis and N. brasiliensis of complement, antibodies from rats infected with these parasites and several different cell types. The cuticle of the infective larvae and adult worms of both nematode species activates complement via the alternative pathway, but the cuticle of newborn T. spiralis lacks this property initially. As newborn larvae grow, however, the newly formed cuticle in the midregion of their body is able to activate complement. Rats infected with either nematode species produce antibodies to the cuticle of all life cycle stages which show marked specificity to each stage in the life cycle. Whereas the cuticle of T. spiralis reacts evenly over the entire surface both to complement and to antibodies, the reaction of the cuticle of N . brasiliensis to either reagent is patchy. Infective larvae of N. brasiliensis were killed in vitro in the presence of complement, by neutral red-positive peritoneal macrophages which were nonadherent to plastic. The infective and newborn larvae of T. spiralis were killed by eosinophil-enriched cell populations and antibodies. The speed of eosinophil killing of the T. spiralis larvae was enhanced when the serum was freshly collected and when the eosinophil suspension also contained neutral red-positive nonadherent macrophages. Newborn larvae of T. spiralis and infective larvae of N . brasiliensis assumed a rigid appearance at death. Infective larvae of T. spiralis burst, extruding their internal organs through their cuticle weakened by antibodies and the cells.
The generalized hematopathology frequently found in animals infected with vector-borne pathogens may maximize transmission by enhancing the ability of vectors to locate blood in infected hosts. We tested this idea of mutualism between parasite and vector by comparing duration of probing of mosquitoes feeding on noninfected and on malaria-(Plasmodium chabaudi) or arbovirus-(Rift Valley fever virus) infected animals. We found that median duration of probing (blood location) on infected rodents was reduced by at least 1 min as compared to noninfected rodents. This enhanced ability of vectors to locate blood, possibly caused by parasite-disrupted hemostasis, may be a common feature of vector-borne diseases.Blood-feeding arthropods must feed rapidly in order to minimize the risks associated with host contact. The time taken by arthropods to locate blood vessels during probing represents an important determinant in their feeding success. Many arthropod vectors of blood-borne diseases secrete antihemostatic saliva that enhances blood vessel location and reduces duration of vector-host contact (1-3). If blood-borne parasites impair hemostasis, blood vessel location by vectors might be further enhanced and transmission might be facilitated. Interestingly, coagulopathy, with marked thrombocytopenia, commonly accompanies infections by vector-borne pathogens (4-9). The consequence of this coincidence between a crucial need by vectors and a prominent feature of infection may be to promote parasite transmission. Such concurrence would also suggest mutualism between vector and parasite. This study sought to determine whether mosquitoes exposed to malaria-or arbovirus-infected hosts located blood faster than those exposed to noninfected hosts. MATERIALS AND METHODSMosquito (Aedes aegypti, Bahama strain) rearing procedures (10) and methods for measuring duration of mosquito probing (2) have been described. Briefly, duration of probing represents the time mosquito stylets remain in the skin until appearance of blood in the midgut. The results are then ranked and plotted cumulatively.BALB/c mice were infected with 105 erythrocytes parasitized with Plasmodium chabaudi (clone PC-7 of the IP-PCI strain) and monitored daily for parasitemia. Animals were used in experiments when parasitemia ranged from 30% to 80%. Mice were anesthetized with a mixture of ketamine and xylazine.Origin of the Rift Valley fever (RVF) virus strain (Zagazig Hospital, 501) and methods of infection and assay have been described (11). Viremias ranged from 103 3 to 108.1 plaqueforming units/ml of blood. Hamsters were anesthetized with ketamine and xylazine. RESULTS First, we compared duration of probing by Ae. aegypti exposed to mice infected with P. chabaudi to those exposed to noninfected mice. Eight mosquitoes were tested per mouse, 12 mice per treatment. The median duration of probing by mosquitoes exposed to infected mice was 71 sec as compared to 147 sec for those exposed to noninfected mice (Fig. 1). A contingency table analysis of the results, gr...
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