The American Journal of Tropical Medicine and Hygiene - Volume 31, Issue 5, 1982

This is the first reported case of congenital double malaria infection. In San Francisco, California, a 6-week-old infant presented with Plasmodium vivax and P. malariae infections. Although the child had not traveled, the mother had recently immigrated from an area north of Bombay, India. Reasons for the delay in onset of the infant's symptoms are given.

During the months April–June and October–November 1980, a survey was conducted among Indochinese refugees arriving in California to assess the prevalence of malaria. During the two study periods, 3,433 refugees were met and 3,289 (95.8%) of the arriving refugees were screened for malaria by examining thick blood smears and by indirect fluorescent malaria antibody tests of blood absorbed on filter paper. Examination of the blood smears showed that the overall patency rates were 1.7% and 0.6% for the first and second surveys, respectively. The Cambodian refugees and refugees from camps in Thailand had the highest patency rate in the first survey. In the second survey, the Cambodian refugees and refugees from camps in Indonesia had the highest patency rate. The average malaria seropositivity rate was 15% in the first and 13.6% in the second survey. The Laotian refugees had the highest rate of malaria seropositivity in both surveys. Plasmodium vivax was the most commonly identified species in blood examination, while a higher rate of seropositivity to P. falciparum was found in both surveys. This study indicates that the malaria infection rate was at least 1.7% based on blood smear examination but might be as high as 45% based on serologic examinations. The results of this study when combined with malaria surveillance indicate that the likelihood of introduced malaria in the United States from the Indochinese refugees is low.

The chloroquine sensitivity of Plasmodium falciparum isolates from infected persons living in Kisumu and Malindi, Kenya, was determined in vivo and in vitro. There was no evidence of chloroquine resistance in 217 patients with P. falciparum infections who underwent standard W.H.O. 7-day in vivo tests. In 71 extended 35-day in vivo tests parasitemia recurred in 14 patients on days 21, 28, or 35. Parasites isolated from these 14 persons during the following period were tested in vitro. Eight tests were successful and showed the isolates to be chloroquine sensitive in vitro, suggesting that the recurrence of parasitemia resulted from reinfection rather than resistance. Macro in vitro tests were done on an additional 67 infected persons, 11 of whom also had sensitive 7-day in vivo tests. Chloroquine resistance was not demonstrated in vitro. In Malindi 100% of isolates were inhibited by a chloroquine concentration of ⩽0.75 nmol/ml blood and 80% by ⩽0.5 nmol as compared with 69% and 27.3% respectively of those from Kisumu. These data from individuals living in malarious areas of Kenya contrast with continuing reports of proven chloroquine-resistant P. falciparum malaria in non-immune visitors who acquired their infections in Kenya.

Fansidar®, quinine, and combinations of the two were evaluated as therapy in 173 cases of falciparum malaria in Royal Thai Army soldiers. Falciparum malaria acquired in the area of the Thai-Khmer border, by military units under Fansidar prophylaxis, has proven refractory to Fansidar therapy. Concurrent use of a single drug as a routine chemoprophylactic and as first-line therapy appears to be inappropriate in this case. Feasible alternatives for either role, however, are not readily available.

Three recently isolated Thai strains of Plasmodium falciparum were tested in vitro for their response to pyrimethamine, sulfadoxine, and both compounds in combination. One isolate, FCK, was moderately tolerant to pyrimethamine whereas FCM3 and FCM5 were not affected by this compound at serum level, being 100 times less responsive than a sensitive strain from the Gambia when tested similarly. This low degree of response is evidently due to drug resistance. Sensitivity to sulfadoxine was low in the Thai isolates, but was also lower than expected in the Gambian strain. Possible causes of the poor response are discussed. Pyrimethamine in combination with sulfadoxine showed a synergistic effect; the effective doses were reduced by ten and three times, respectively.

Infectious agents must acquire iron from their host to survive, and iron deficiency has been reported to protect against malaria in humans. We have tested the the susceptibility of Plasmodium falciparum to iron deprivation by studying the effect of desferrioxamine (DF), a specific iron chelating agent, on parasite growth in an in vitro culture system. We have found that DF inhibits the growth of P. falciparum at concentrations readily achievable in vivo, by a mechanism that may involve interference with the completion of schizogony.

NIH-white mice were injected with varying doses of Plasmodium vinckei or Plasmodium yoelii lethal via the hind footpad (FP), intraperitoneal (IP), or subcutaneous (SC) routes. Survival was dependent on the dose of the inoculum and route of injection. Injection via the IP and SC routes led to higher mortality than the FP route. The results showed that at a dose of 104 parasitized erythrocytes injected IP led to 100% mortality, whereas the same dose injected via the FP route gave protection.

We describe a patient with kala azar who presented with retinal hemorrhages. The hemorrhages resolved during treatment with pentavalent antimony.

A Colombian phenotype, laboratory-born squirrel monkey, Saimiri sciureus, was found to be congenitally infected with biologically proven Trypanosoma cruzi. The parasite was observed in blood smears and by xenodiagnoses of the mother and the offspring, and the isolates produced infection in mice and amastigotes in VERO tissue culture cells. The finding was accidental; both animals were healthy. Tissues of the mother did not show macro-microscopic evidence of T. cruzi infection and the electrocardiograph of the offspring was normal. This seems to be the first report of congenital T. cruzi transmission in an otherwise healthy non-human primate.

The results reported here show that a clone of a South American Trypanosoma cruzi human isolate has an epitope antigenically related to sarcoplasmic reticulum adenosine triphosphatase preparations (SRA), an enzyme implicated in the contraction-relaxation cycle of striated muscle. The antigenic determinant of T. cruzi, which is cross-reactive with SRA, is located in the interior of the parasite. No surface cross-reaction was detected with intact, freely swimming flagellates. Indeed, the degree of cross-reactivity was increased when T. cruzi microsomes were trypsinized, probably resulting in further exposure of the normally internal cross-reactive epitope.

The clinical and parasitologic aspects of filariasis were investigated in 459 inhabitants of a South Pacific island endemic for subperiodic Wuchereria bancrofti filariasis. Episodes of filarial fevers, usually with concomitant lymphangitis and/or lymphadenitis, were experienced by 26%. Lymphobstructive lesions, manifest in the later decades of life, were present in 12 with elephantiasis and 24 with hydroceles. Microfilaremia was detectable by membrane filtration of 1 ml of blood in 33% of persons, with a quarter of these having less than 50 microfilariae/ml. Microfilaremia and filarial fevers were more frequent in males than females and in residents of the most inland villages. Neither presence nor magnitude of lymphadenopathy correlated with other manifestations of filariasis except that markedly enlarged inguinal-femoral nodes were more common in those with elephantiasis or hydroceles. A history of filarial fevers did not correlate with presence of microfilaremia. Over 70% of adults had microfilaremia and/or historical or physical manifestations of filariasis. The absence of detectable microfilaremia in many residents with clinical evidence of filariasis and the presence of asymptomatic microfilaremia emphasize the limitations in relying only on microfilaremia rates or clinical findings in the study of the prevalence or manifestations of filarial infection.

Sixty-eight individuals from a Pacific island hyperendemic for subperiodic bancroftian filariasis were selected from a larger study population to include the entire clinical spectrum of filarial infection in that region and also an “endemic control” group without clinical or parasitologic evidence of filarial infection. Analysis of their blood leukocyte and humoral immune responses yielded the following major findings: 1) levels of specific antifilarial antibodies of three different immunoglobulin classes (IgG and IgM measured by ELISA and IgE determined by radioimmunoassay) were significantly greater in the “endemic control” population than in the patients with filariasis, an observation true for both children and adults; 2) the endemic controls also had significantly higher levels of serum IgM and C3 than did the filariasis patients; 3) while individuals with “filarial fevers” and “chronic (lymphatic) pathology” did have significantly lower IgG antibody responses to filarial antigen than the controls, the lowest antibody levels were found in the patients with microfilaremia; 4) symptomatic patients (i.e., those with filarial fevers or lymphatic obstruction) regularly showed higher specific antibody responses to filarial antigens than asymptomatic, infected individuals, although the difference did not reach statistical significance. These findings are in concert with our previously reported, intriguing observation that lymphocyte proliferative responsiveness to filarial antigens was much greater in individuals of the ‘non-infected’ endemic control population than in patients with filariasis; furthermore, they indicate the important issues that must be approached and resolved to define the immunologic determinants leading both to the various filarial clinical syndromes and to protective immunity.

A longitudinal study was performed in an island, endemic for Bancroftian filariasis, by blood survey and skin test from the beginning of a filariasis control campaign in 1967 through 1980. The initial microfilarial rate of 13.2% was successfully reduced to almost 0 by 1970, by the selective administration of diethylcarbamazine to microfilaria positives. The age distribution of skin-test positivity changed year by year, especially in the younger age groups. A marked reduction was seen in the positive rate in the 0- to 9- and 10- to 19-year-old age groups. The change of skin reactivity for all islanders was evaluated, and revealed a gradual decrease in the wheal-size over the observation period.

Prevalence rates of heartworm in coyotes was estimated for five northern California counties by examining hearts of coyotes obtained from federal or private trappers. Prevalence rates range from 8.3–27.3%, but the proportion of infected coyotes can vary between two regions of the same county. In general, it seems that higher infection rates are found in the foothill regions of the Coastal Range and Sierra Nevada, decreasing towards the floor of the Sacramento Valley as well as at higher elevations. The use of coyotes as sentinel animals for detecting natural foci of transmission is postulated.

Sera from 58 cases of confirmed human trichinosis were examined over an 11-month period. The enzyme-linked immunosorbent assay (ELISA) was used for the detection of class-specific serum antibodies (IgG, IgM, IgA, IgE) and for total serum IgE. The indirect immunofluorescent test served as reference technique. The ELISA proved to be more sensitive. Specific IgG antibodies were detected by ELISA in 100% of the clinical cases. Both IgG and IgM were demonstrable throughout the observation period of 11 months. Specific serum IgA was seen in 62% of the patients during the first 3 months, presumably the result of stimulation of the immune system by the adult worms in the intestine. Specific serum IgE was seen in a few cases only at the onset of the disease. Total serum IgE levels were elevated in 32% of the patients in the first month of the disease and in 17% after 11 months, compared to 10% of healthy individuals.

Praziquantel is a newly developed drug effective in the treatment of schistosomiasis. In order to assess the efficacy and toxicity of praziquantel in the treatment of Schistosoma mekongi, 11 infected Laotian refugees, all belonging to a single extended family, were treated in a double-blind crossover trial with praziquantel and placebo. Initially, one group of five received praziquantel 60 mg/kg body weight in three divided doses orally while the remainder received an identically appearing placebo. Patients were evaluated clinically before, during and following therapy for 2 days. After 2.5 months the patients were re-evaluated and subjected to the opposite treatment, and final follow-up took place 5–7 months later. Three other patients were treated using an open protocol. All but one person was cured (91%). This patient failed to show a decrease in egg excretion 2.5 weeks after praziquantel therapy and was lost to follow-up thereafter. Side effects were common and consisted primarily of abdominal pain, malaise, and fever. These were generally mild and transient. No abnormal laboratory findings were associated with praziquantel therapy. At the final evaluation 6/6 patients with initial hepatomegaly showed a decrease in liver size.

Capuchin monkeys were studied for 7 months after exposure to Schistosoma mansoni or to either a Japanese or a Philippine strain of Schistosoma japonicum. The number of eggs present in the tissues and passed in the feces of S. mansoni-infected monkeys correlated well with the number of worm pairs recovered. Monkeys infected with the Philippine strain of S. japonicum passed large numbers of eggs in the feces and the number of these eggs correlated well with the number of worm pairs present. In monkeys infected with the Japanese strain of S. japonicum, fewer eggs were passed in the feces and there was little correlation with the number of worm pairs. Schistosome eggs were found predominantly in the small intestine in monkeys infected with the Philippine strain and predominantly in the colon in monkeys infected with the Japanese strain. The patterns of egg excretion in the feces and egg distribution in the tissues contrast with the patterns we recently described in rabbits, in which animals infected with the Philippine strain passed few eggs in the feces and showed a high proportion of tissue eggs in the colon. A single host species is thus shown to be inadequate to characterize the behavior of a schistosome strain.

Isolated cases of schistosomiasis were discovered on stool examination among Cambodian refugees residing in Thailand. Further epidemiologic investigations were conducted on a sample of 5,085 Cambodian refugees in the Ban-Kaeng holding center, using the intradermal skin test as a screening device to determine the prevalence of this disease. A positive diagnosis of Schistosoma mekongi was confirmed in 17 of those examined by recovery of eggs in the stool. The prevalence of schistomiasis in the Bang-Kaeng camp was 3.3 cases/1,000 population. All positive cases came from geographic areas in Cambodia where schistosomiasis has not been previously reported, indicating that schistosomiasis in Cambodia is currently more widespread than generally believed.

Mechanically transformed schistosomula of Schistosoma mansoni exposed to mouse, rat or human inactivated immune sera (coated schistosomula) and then injected intravenously into CBA mice were recovered from their lungs in smaller numbers than were schistosomula exposed to normal sera, immune sera absorbed with S. mansoni tegument, or sera from mice bearing unisexual cercarial infections and displaying moderate titers of lethal antibodies. The reduction of the number of coated schistosomula recovered from the lungs, as well as the lethal effect in vitro, were mediated by 7S fraction of the immune sera. Decomplementation (by Cobra Venom Factor) or irradiation (650 R, 1, 3, and 5 days before injection) of recipient mice, increased the number of coated schistosomula recovered from their lungs.

Encounters between axenically transformed sporocysts of the Puerto Rican 1 strain of Schistosoma mansoni and hemocytes and plasma components of susceptible “M line” and resistant 10-R2 and 13-16-1 strains of Biomphalaria glabrata were studied in vitro. After 24 hours of incubation in susceptible hemolymph components, 94.4% of 36 observed sporocysts retained normal structure, whereas 91.6% of 48 sporocysts were destroyed after 24 hours of incubation in resistant hemolymph components. Sporocysts preincubated for 6 hours in susceptible plasma were destroyed when subsequently incubated with resistant hemocytes in susceptible plasma. Sporocysts preincubated in resistant plasma were not destroyed when subsequently incubated with susceptible hemocytes and plasma. Susceptible hemocytes preincubated in resistant plasma, and then incubated for 24 hours with sporocysts in the presence of susceptible plasma were incapable of inflicting damage. The simultaneous incubation of sporocysts with susceptible hemocytes and resistant plasma produced variable results. The predominant trend was sporocyst destruction in five replicates and lack of substantial damage in six replicates. Results of these and previous experiments imply that differences between susceptible and resistant strains of snails in their ability to destroy sporocysts in vitro can be attributed primarily to differences in their hemocytes, although plasma factors may alter these responses in some cases. The results also suggest that if sporocysts do acquire a coat of host plasma components, this strategy is by itself insufficient to account for the persistance of sporocysts in susceptible snails.