The American Journal of Tropical Medicine and Hygiene - Volume 15, Issue 2, March 1966

The American Society of Tropical Medicine was established in Philadelphia, March 9, 1903 by a small group of well known clinicians who were members of the College of Physicians of Philadelphia. Of the 28 who signed the Charter, nine were members of the Jefferson Medical College Faculty. At the first public meeting, James Carroll, Surgeon, U. S. Army, addressed the Society on the subject “The etiology of yellow fever.” Sixty-two years later, our Society can contemplate with pride the enormous contributions made during the past six decades in the field of tropical medicine by the membership of our current organization and its parent societies, particularly in the field of control of communicable diseases.

At the beginning of the twentieth century, communicable diseases were exacting a colossal toll of life in all areas of the world, but in the tropics and subtropics the losses were truly devastating.

Histological skeletal muscle lesions found in the acute stage of Chagas' disease were studied in mice.

Almost all the mice infected with Trypanosoma cruzi developed a “polymyositis” with interstitial and parenchymatous lesions. The complete histological picture of the myositis was characterized by mononuclear cell infiltration of the perimysium, waxy degeneration of fiber segments, the presence of pseudocysts and granulomatoid foci in the muscle fibers, panarteritis of small intramuscular vessels, and regeneration of the muscle fibers. The infiltrates and the phenomena of waxy degeneration were the changes most constantly seen. Not all of the damaged muscles showed a florid histological picture. In many instances there was a non-specific myositis without pseudocysts and granulomatoid foci. The waxy degeneration and the interstitial infiltration very often presented no direct relationship to the presence of parasites. In the differential diagnosis of chagasic myositis, other necrobiotic and parasitic myosites must be considered.

Alterations were studied in 857 samples of skeletal muscle from mice experimentally infected with Trypanosoma cruzi and Schistosoma mansoni. In some of the animals the T. cruzi infection was followed up to 126 days. The presence of S. mansoni infection had no apparent effect on the picture of the “polymyositis” caused by T. cruzi infection. There was an apparent relationship between the percentage of damaged muscles and the number of trypanosomes inoculated. Schistosome infection that was not associated with trypanosomiasis caused minor muscle lesions in only 5 of the 107 muscles examined. These consisted of intramuscular panarteritis and perivascular lymphocytic infiltration in the perimysium.

The rates of spontaneous death in the several experimental groups suggested that T. cruzi infection may have had a protective effect against S. mansoni infection.

The effect of chloroquine and pyrimethamine on visceral leishmaniasis in the hamster was studied using the screening method of Stauber et al. Neither pyrimethamine at 10 mg/kg/day for 6 days or chloroquine at 100 mg/kg/day for a total of 12 days inhibited the multiplication of Leishmania donovani in the hamster liver. However, reasons are presented for using caution in interpreting the negative results obtained in this study.

A qualitative and quantitative evaluation of the indirect fluorescent antibody test for toxoplasmosis was made by comparison with methylene blue dye test results on 1,000 serum specimens. Over 95% agreement between the two tests was obtained in qualitative results and excellent agreement in titers was also noted, although the fluorescent antibody technique tended to yield higher titers. This test appears to equal the dye test in specificity and sensitivity and eliminates the need for living organisms and human serum accessory factor.

A study of schistosomiasis mansoni was performed in 9 marmosets. Six were exposed to a predetermined number of cercariae obtained from snails naturally infected with Schistosoma mansoni in Bahia, Brazil. Eggs were first observed in the feces 15 weeks after exposure; the ratio of worms to cercariae was low, averaging 5.2%, and the worms were stunted. In an additional experiment, worms isolated from marmosets 7.5 weeks after exposure to cercariae of S. mansoni were significantly smaller than worms isolated at the same time from a group of simultaneously exposed Swiss albino mice. None of the marmosets showed ill effects from the infection. It appears that the marmoset is resistant to infection with S. mansoni.

Of 54 patients infected with Schistosoma haematobium, 65%, 49%, and 47% remained urinary carriers of Salmonella typhi and S. paratyphi A infections 3, 6, and 12 months, respectively, after initial diagnosis of bacillary enteric fever. Of 21 patients with typhoid or paratyphoid-A fever but no schistosomiasis, none became urinary carriers. The chronic enteric urinary carriers among the schistosomal patients had a high incidence of radiologically detectable obstructive lesions of the urinary tract (90% of 21 patients at 12 months) in contrast to the non-carriers among the schistosomal patients (none of 11). The incidence of the urinary carrier state was 51% in paratyphoid-A cases and 10% in typhoid cases, and was higher in children than in adults. Schistosomal lesions of the urinary tract appear to predispose toward the development of the urinary carrier state of the bacillary infections, and this suggests that effective therapy of the carrier condition may require surgical removal of the urinary obstructions in such cases and indicates the value of schistosomiasis-control measures in the prevention of acute and chronic salmonellosis.

A study was made of the necrotizing and healing arteritis in 10 patients who had developed schistosomal cor pulmonale. The necrotizing vasculitis was classified into two groups: (1) produced directly by the Schistosoma mansoni eggs and of probable allergic origin and (2) not directly related to the presence of eggs and apparently connected with either hypersensitive reactions caused by antigenic substances in the circulating blood or with a nonspecific reaction to hypertension. The widespread healed arteritis is described and an attempt is made to relate the organization and recanalization of hyaline thrombi to the development of plexiform structures.

A case of primary renal echinococcosis in a 22-year-old Italian male is presented. The cyst had ruptured into the renal pelvis and had caused the passage of jelly-like material in the urine, associated with renal colic and dysuria.

Intradermal tests utilizing an aqueous extract of Echinococcus multilocularis cyst material were performed on 104 individuals living in Uruguay for evaluation of the skin test. In this group, 43 individuals had proven hydatid disease and 61 were normal or had non-hydatid diseases. Antigens containing 0.012 to 0.401 mg N/ml were used. Highest specificity was obtained with skin test antigens which contained 0.012 to 0.015 mg N/ml.

Sera from 124 individuals were collected in Uruguay. All but four of the skin-test group were included. Each serum was tested by the indirect hemagglutination, bentonite flocculation and latex agglutination tests. None of the sera in the non-hydatid group reacted in the hemagglutination test and only a few reacted in the bentonite and latex tests. The sensitivity of the serologic tests in patients infected with E. granulosus varied from 82% for serum from individuals with liver cysts to 33–50% for serum from patients with lung cysts.

The occurrence of spurious infection with eggs of the small liver fluke, Dicrocoelium hospes, is described in two jaundiced patients and three other patients. It was found that the patients had been eating infected liver beef in their hospital diet and intermittently passing eggs. D. hospes has been found to be a common parasite of cattle in Ghana and it is suggested that true infections in man may also occur. Little information regarding D. hospes is available and the life cycle has not been worked out as yet, but is probably similar to the closely related D. dendriticum.

The finding of microfilariae in lung tissue from patients with eosinophilic lung is reported and the histopathological appearances are described.

In general, the results of a serological survey of 1420 sera representing 34 species of primates agree with previous reports in the literature and suggest that there is either very little leptospiral infection in these animals in Nature, or that their antibodies formed in response to leptospiral infection do not persist for any appreciable length of time. Fourteen of the 19 serologic reactors among baboons (Papio sp.), 9 of the 48 reactors among chimpanzees (Pan troglodytes), 2 of the 3 reactors among the patas monkeys (Cercopithecus patas), and the one reactor among the marmosets (Oedipomidas oedipus) showed antibodies agglutinating Leptospira ballum, a serotype not known to occur in the native habitat of these animals, but prevalent in the mouse in the United States. In addition, at least two of the L. icterohemorrhagiae infections in the group of chimpanzees examined are known to have occurred while the animals were in captivity; this serotype has also been demonstrated in the mouse and many other small mammals in the United States. All four of these primate species are known to catch and eat insects and small mammals.

The absence of detectable leptospiral agglutinins in all except one of the small group of New World primates examined confirms the previous published and unpublished findings of other workers. To date, there is no evidence of leptospiral infections in Nature among any of the New World primates.

A review has been presented of the isolation of the first of the viruses in the California encephalitis complex and the sequence of the reported isolations of other members of the group in the United States, Canada, Africa, Europe and Trinidad. Involved are lapses of many years between early isolations in the United States and an interval of essentially twenty years in the San Joaquin Valley of California, despite a constant and increasingly vigorous search. Most viruses of the group have laboratory characteristics quite similar to those of the prototype, but their antigenic mosaic is highly varied suggesting that this virus is quite unstable. In addition to five previously recognized viruses in the group, two of which were from the United States, there now appear to be at least seven antigenic types in the United States in the viruses so far compared in this laboratory. The prototype virus measures about 50 mµ by electron microscopy and is observed only in the cytoplasm of cells. Clinical cases, rarely recognized in previous years, have recently been reported in increasing numbers from many parts of the United States based on serological testing. The first epidemic was recognized in 1964 in Indiana. Virus isolation has been reported from one fatal case of encephalitis; otherwise all virus isolations have been from arthropods, chiefly mosquitoes, and from hares and rabbits. The cycle in nature is probably principally from small mammals to mosquitoes and back to the small mammals, while man appears to be an accidental dead end host. There is no evidence of involvement of birds, an apparently highly resistant group of vertebrates.

Sera collected from 60 selected South Florida patients with undiagnosed infectious disease in 1961, 1962, and 1963 were studied in hemagglutination-inhibition tests with 22 selected arboviruses. This was done in order to determine whether or not any one of the viruses caused the disease of each patient and to determine the HI antibody status of representative South Florida residents against a spectrum of arboviruses. Among the 60 patients, 11 had encephalitis, 39 had aseptic meningitis, and the illnesses of the remaining 10 were characterized as undifferentiated febrile illnesses.

Hemagglutination-inhibition antibodies were observed to 10 arboviruses in one or more of the late sera from nine patients: three were cases of encephalitis, three were aseptic meningitis and three were classified as undifferentiated febrile illnesses. The antibodies were to eight Group B viruses including bat salivary gland, Bussuquara, dengue type 2, Ilheus, Modoc, MVE, Powassan, and SLE, as well as Bunyamwera, Guaroa, Tensaw, and Tahyna. Further tests with two or more sera from those nine patients having significant levels of HI antibody revealed a significant rise in antibody titer in four patients consistent with a definitive diagnosis, at least by arbovirus grouping.

No HI antibodies were detected in sera from the 60 patients to the Group A viruses of Aura, EEE, Highland J, Una, VEE, and WEE, nor to the Group C viruses of Caraparu, Marituba, and Oriboca. Also, no HI antibodies were detected among the entire group of sera against Bussuquara, Modoc, and Powassan viruses, except for one serum which was broadly reactive to all Group B viruses used and sera from two patients having titers of 1:40 or 1:20 to two of these viruses.

Two patterns of serological reactivity were observed in cases of Group B arbovirus infection occurring in South Florida, one associated with St. Louis encephalitis and the other with dengue.

During 1961, antibodies neutralizing eastern equine encephalitis (EEE) virus were found in plasmas of man and resident wild birds in southern Mexico at Tlacotalpan, Veracruz on the tropical eastern coast and at Coatetelco, Morelos on the central upland plateau. Antibodies neutralizing western equine encephalitis (WEE) virus were detected in plasmas from man, resident wild birds and swine at Tlacotalpan, but only from migratory birds at Coatetelco. Maximal prevalence rates for these antibodies were 2% in man and 6% in adult birds. No viruses were recovered by inoculation of suckling mice with plasmas from 88 permanently resident and 88 migratory birds at Tlacotalpan; 72 and 61 plasmas were also negative in hamster kidney and chicken embryonic cell cultures respectively. Because most humans were without detectable neutralizing antibody, a major future amplification of EEE or WEE virus activity in these regions could result in encephalitis epidemics.

A method for producing large volumes of mouse ascitic fluids with high viral antibody titers by the use of adjuvant in combination with Sarcoma 180 cells is described. Ascitic fluids so produced reacted specifically with the viruses to which they were prepared. In cross complement-fixation and hemagglutination-inhibition tests, none of 26 ascitic fluids prepared to individual viruses and of nine polyvalent ascitic fluids reacted with antigens outside the recognized or artificial grouping. Satisfactory neutralization indices were obtained with the ascitic fluids tested.

Dogs experimentally infected with the Trinidad strain of Venezuelan equine encephalomyelitis (VEE) virus served as donor hosts for the infection of Aedes triseriatus mosquitoes, 10 percent of which then transmitted the disease to guinea pigs by bite 21 days later. A. aegypti which fed simultaneously did not become infected.

The infection in dogs caused a frank febrile response and hemagglutination-inhibition antibody formation. Significant virus concentrations were demonstrated in the blood, brain, and testicle. Although death occurred in 6 of the 10 challenged animals, overt signs of illness were minimal. The two uninoculated dogs which were in contact with the challenged dogs became infected, but neither died.

Microscopic study of the brains disclosed various alterations, which, although not diagnostic, are considered compatible with VEE infection.

A previously undescribed virus has been isolated from Culex spp., Psorophora ferox and sabethine mosquitoes in Trinidad. The name Aruac is proposed for this agent. Aruac virus has not been isolated from any source other than mosquitoes. Neutralizing antibody to the virus has not been demonstrated in human serum. Some of the physical and biological properties of the virus are described.

Nariva virus is a new, ether-sensitive agent isolated on four separate occasions from rodents, Zygodontomys b. brevicauda, caught in Bush Bush forest in the Nariva swamp, eastern Trinidad, in 1962 and 1963. Identification of the virus and its behavior in various animals and tissue cultures are reported. Limited studies disclose no evidence of human infection with Nariva virus. Twenty-three of 29 Zygodontomys captured during the period the isolations were made had Nariva virus neutralizing antibodies.