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Geoffrey M Jeffery

Publications and source records attributed to Geoffrey M Jeffery.

9 recordsLinked to original sources

Plasmodium ovale: parasite and disease.

Humans are infected by four recognized species of malaria parasites. The last of these to be recognized and described is Plasmodium ovale. Like the other malaria parasites of primates, this parasite is only transmitted via the bites of infected Anopheles mosquitoes. The prepatent period in the human ranges from 12 to 20 days. Some forms in the liver have delayed development, and relapse may occur after periods of up to 4 years after infection. The developmental cycle in the blood lasts approximately 49 h. An examination of records from induced infections indicated that there were an average of 10.3 fever episodes of > or = 101 degrees F and 4.5 fever episodes of > or = 104 degrees F. Mean maximum parasite levels were 6,944/microl for sporozoite-induced infections and 7,310/microl for trophozoite-induced infections. Exoerythrocytic stages have been demonstrated in the liver of humans, chimpanzees, and Saimiri monkeys following injection of sporozoites. Many different Anopheles species have been shown to be susceptible to infection with P. ovale, including A. gambiae, A. atroparvus, A. dirus, A. freeborni, A. albimanus, A. quadrimaculatus, A. stephensi, A. maculatus, A. subpictus, and A. farauti. An enzyme-linked immunosorbent assay has been developed to detect mosquitoes infected with P. ovale using a monoclonal antibody directed against the circumsporozoite protein. Plasmodium ovale is primarily distributed throughout sub-Saharan Africa. It has also been reported from numerous islands in the western Pacific. In more recent years, there have been reports of its distribution on the Asian mainland. Whether or not it will become a major public health problem there remains to be seen. The diagnosis of P. ovale is based primarily on the characteristics of the blood stages and its differentiation from P. vivax. The sometimes elliptical shape of the infected erythrocyte is often diagnostic when combined with other, subtler differences in morphology. The advent of molecular techniques, primarily PCR, has made diagnostic confirmation possible. The development of techniques for the long-term frozen preservation of malaria parasites has allowed the development diagnostic reference standards for P. ovale. Infections in chimpanzees are used to provide reference and diagnostic material for serologic and molecular studies because this parasite has not been shown to develop in other nonhuman primates, nor has it adapted to in vitro culture. There is no evidence to suggest that P. ovale is closely related phylogenetically to any other of the primate malaria parasites that have been examined.

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A retrospective examination of the effect of fever and microgametocyte count on mosquito infection on humans infected with Plasmodium vivax.

A retrospective examination was made of archival data collected between 1940 and 1963 on the infection of mosquitoes with the St. Elizabeth strain of Plasmodium vivax. Patients were undergoing malariatherapy for the treatment of neurosyphilis. A total of 845 lots of Anopheles quadrimaculatus mosquitoes were fed during primary infections and 76 during secondary infections. Average percentage infection during the primary infection was 56.55% versus 49.83% during the secondary infection. There appeared to be no relationship between microgametocye density, asexual parasite count, and percentage infection. However, very high fevers appear to have a significant effect on infection rates. Persons with fever > or = 105 degrees F showed the lowest rates of infectivity regardless of parasitemia; persons with moderate (101-104.8 degrees F) fever produced somewhat higher rates, and persons with no fever had the highest levels of infection at all parasitemia levels greater than 1,500/microL

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A retrospective examination of reinfection of humans with Plasmodium vivax.

A retrospective examination was made of archival data collected between 1940 and 1963 to determine the impact of reinfection of patients with Plasmodium vivax with homologous and heterologous strains of the parasite. Following reinfection of 14 patients with a homologous strain, the geometric mean maximum parasite count was reduced from 9,101/microL during the primary infection to 998/microL and the geometric mean daily parasite count for the first 20 days was reduced from 923/microL to 16/microL. Following reinfection of 22 patients with heterologous strains of P. vivax, the geometric mean maximum parasite count was 8,460/microL during the primary infection versus a secondary level of 9,196/microL and the geometric mean daily parasite count decreased from 847/microL/day to 335/microL/day. Reductions in fever episodes > or =101 degrees F and > or = 104 degrees F appeared to be a more sensitive measure of clinical immunity. Fever episodes > or =104 degrees F in patients with homologous strain reinfections decreased from 1.92 episodes per week to 0.18 compared with 1.24 to 0.57 in patients with heterologous infections. Fever episodes > or =101 degrees F decreased from 2.98 to 0.60 in the homologous strain compared with 2.08 to 1.07 for the heterologous infections. The average maximum fever temperature in the homologous group was 106 degrees F during the primary infection versus 103.4 degrees F for the secondary infection compared with 105.8 degrees F during the primary infections versus 105.6 degrees F for the secondary infection in the heterologous patients.

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A retrospective examination of mosquito infection on humans infected with Plasmodium falciparum.

A retrospective examination was made of archival data collected between 1940 and 1963 on the infection of mosquitoes with Plasmodium falciparum. Patients were undergoing malariatherapy for the treatment of neurosyphilis. A total of 913 lots of Anopheles quadrimaculatus and An. albimanus were fed on 173 patients. Mosquito infection continued to occur in a few patients beyond 200 days of patent parasitemia. The primary period of mosquito infection occurred during the first 20 days of gametocytemia. Of the 311 lots of mosquitoes fed during this period, 209 (67.20%) were infected, and of these, 163 had greater than 50% of the mosquitoes in the lots infected with at least one oocyst. During secondary periods of gametocytemia, 293 (78.76%) of 372 lots of mosquitoes were infected. The highest percentages of mosquitoes were infected from four days before to four days following peak gametocyte density. Mosquito infection rates were similar to those seen in studies with splenectomized Aotus monkeys experimentally infected with P. falciparum.

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A retrospective examination of anemia during infection of humans with Plasmodium vivax.

A retrospective examination was made of archival data on 98 patient episodes of infection with Plasmodium vivax occurring over a period of 4-11 weeks to document changes in hemoglobin (Hb) concentrations associated with continuing parasitemia. The mean percentage change in the Hb concentration for each of the 10 seven-day intervals was -13.4, -10.9, -4.8, 0.12, 0.94, 4.0, 0.69, 11.6, 2.4, and 8.3, respectively. An equilibrium appeared to be established between weeks 4 and 6. Decreases in Hb concentrations were greatest following the first week of parasitemia. Total restoration to preinfection levels did not occur during persistent parasitemia.

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Plasmodium vivax blood-stage dynamics.

We examine the dynamics of parasitemia and gametocytemia reflected in the preintervention charts of 221 malaria-naive U.S. neurosyphilis patients infected with the St. Elizabeth strain of Plasmodium vivax, for malariatherapy, focusing on the 109 charts for which 15 or more days of patency preceded intervention and daily records encompassed an average 98% of the duration of each infection. Our approximations of merogony cycles (via "local peaks" in parasitemia) seldom fit patterns that correspond to "textbook" tertian brood structures. Peak parasitemia was higher in trophozoite-induced infections than in sporozoite-induced ones. Relative densities of male and female gametocytes appeared to alternate, though without a discernably regular period. Successful transmission to mosquitoes did not depend on detectable gametocytemia or on absence of fever. When gametocytes were detected, transmission success depended on densities of only male gametocytes. Successful feeds occurred on average 4.7 days later in an infection than did failures. Parasitemia was lower in homologous reinfection, gametocytemia lower or absent.

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A retrospective examination of sporozoite-induced and trophozoite-induced infections with Plasmodium ovale: development of parasitologic and clinical immunity during primary infection.

A retrospective analysis was made of clinical and parasitologic parameters in patients with induced Plasmodium ovale infection to document the initial clinical and parasitologic response and their subsequent development of clinical and parasitologic immunity, and to determine the effect of previous homologous and heterologous malaria on subsequent infection with this parasite. The prepatent periods were relatively uniform. Eight patients injected with sporozoites that had been stored frozen had a median prepatent period of 14 days (range = 14-20 days). Thirty-five patients infected via the bites of infected mosquitoes had a median prepatent period of 15 days (range = 12-18 days). In eight patients previously infected with P. vivax, the median prepatent period was 16 days. High-intensity fever (> or = 104 degrees F) was frequently seen, with instances of fever > or = 106 degrees F recorded on many occasions. Fever > 101 degrees F and > 104 degrees F occurred for much shorter periods of time than had been observed in patients infected with P. falciparum. Parasite counts > 10,000/microL were infrequent; in most patients, such parasite counts rarely lasted more than two or three days. Gametocytemia was generally of low density and lasted only a few days. The overall length of the clinical and parasitologic period was much shorter compared with that seen in patients infected with P. falciparum. Previous infection with P. ovale did not prevent reinfection, but resulted in reduced levels of parasitemia and fever. Previous infection with heterologous species of Plasmodium did not prevent infection; some reduction in the frequency and intensity of fever and parasite counts was evident. Previous infection with homologous or heterologous parasites failed to eliminate the production of infective gametocytes. A total of 462 lots of mosquitoes were fed on 67 patients with no previous history of infection. Of these feedings, 168 (36.4%) resulted in infection as determined by the presence of oocysts on the midguts of dissected mosquitoes. As shown, the infection rate increased with the density of gametocytes even though 48 (23.4%) of 205 lots of mosquitoes fed when no gametocytes were detected were infected.

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Extended clearance time after treatment of infections with Plasmodium malariae may not be indicative of resistance to chloroquine.

A retrospective examination was made of archival data on the response of Plasmodium malariae infections in humans to chloroquine. The clearance time for P. malariae was longer than that for P. falciparum and P. vivax. Of 100 P. malariae-infected patients treated with 1,500 mg of chloroquine given over 3 days, 15 had detectable parasites for 7 days, 4 for 10 days, and 1 for 15 days after treatment. Of 17 patients treated intramuscularly with 450 mg of dihydrochloroquine, parasites persisted in 1 patient for 11 days. Of patients with chloroquine-sensitive P. falciparum. 44 cleared parasites by 6 days after treatment; 37 patients with P. vivax infections cleared parasites by day 5. The confirmation of chloroquine resistance may depend on the adaptation of isolates to nonhuman primates in which controlled drug trials can be made.

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Plasmodium malariae infection boosts Plasmodium falciparum gametocyte production.

We analyzed records of malaria therapy patients sequentially or simultaneously inoculated with Plasmodium falciparum and Plasmodium malariae. Gametocyte production was enhanced in P. falciparum by prior or concurrent P. malariae infection but diminished or unaffected in P. malariae by P. falciparum. Conversely, asexual-form production was diminished in P. malariae but unaffected in P. falciparum.

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