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Two cases of gongylonematiasis in common marmosets of two research facilities in Germany are reported. The helminthiasis was transmitted from colony A to colony B by one infected female and within colony B by cockroaches (Blatella germanica). Four of 40 cockroaches examined in colony B were infected with rhabditiform larvae. Clinical signs of disease in the infected animals consisted of intense itching and scratching of the edematous and slightly hyperemic perioral tissues. Histologically the adult helminths lodged predominantly in the mucous membranes of the upper and lower lips; they were less frequently present in the labial cutaneous parts or in the tongue and could not be seen in the esophageal wall, bronchi, or abdominal organs. The helminthic infection probably caused minor to moderate mixed inflammatory infiltrates of the periesophageal connective tissues and intense inflammation of the deep lingual muscular tissues. Lesions of the mucosal membranes of the lips and tongue had predominant accumulations of neutrophilic granulocytes, lymphocytes, and mostly degranulated mast cells with only a few eosinophilic granulocytes. In the cutaneous part of the lips multifocal microabscesses were considered to be secondary lesions from the intense scratching.

Wild measles virus isolated in a marmoset lymphoblastoid B95a cell line induced rashes and Koplik's spots when inoculated parenterally in cynomolgus and squirrel monkeys. Marked leukopenia. associated with transient decrease in the CD4(+)-to-CD8+ T-cell ratio also was induced. Virus growth, as well as histologic lesions of necrosis and giant cell formation, was observed in the lymphoid tissues. Thus clinical signs of acute measles were successfully induced in monkeys by inoculation with cell-culture-grown measles virus. These nonhuman primate models of measles will be useful for study of the pathogenesis of acute measles virus infection in terms of generalized clinical signs of disease, leukopenia, and changes in the lymphocyte subsets.

An outbreak of malignant lymphoma has been observed in one of the baboon (Papio hamadryas) stocks of Sukhumi Primate Center. More than 300 cases in this "high-lymphoma stock" have been registered since 1967. Human T-cell lymphotropic virus type 1 (HTLV-1)-related virus was implicated as the etiologic agent of Sukhumi baboon lymphoma. The origin of this virus remained unclear. Two possibilities were originally considered: the origin could be baboon simian T-cell leukemia/lymphoma virus type 1 (STLV-1) or HTLV-1 (before the outbreak started, some Sukhumi baboons were inoculated with human leukemic material). The third possibility entered recently: interspecies transmission of rhesus macaque STLV-1 to baboons. It was prompted by the finding of very close similarity between STLV-1 991-1cc (the strain isolated from a non-Sukhumi baboon inoculated with material from a Sukhumi lymphomatous baboon) and rhesus STLV-1. To test this hypothesis, we investigated 37 Sukhumi STLV-1 isolates from baboons of high-lymphoma stock by PCR discriminating rhesus type and baboon type STLV-1 isolates. All of them were proved to be rhesus type STLV-1. In contrast, all six STLV-1 isolates from baboons belonging to other stocks or populations were of baboon type. The PCR results were fully confirmed by DNA sequence data. The partial env gene gene sequences of all four STLV-1 isolates from Sukhumi lymphomatous baboons were 97 to 100% similar to the sequence of known rhesus STLV-1 and only 85% homologous with the sequence of conventional baboon STLV-1. Thus, interspecies transmission of STLV-1 from rhesus macaques (or closely related species) to baboons occurred at Sukhumi Primate Center. Most probably this event initiated the outbreak of lymphoma in Sukhumi baboons.

Acquired Immune Deficiency Syndrome (AIDS) is caused by two different Human Immunodeficiency Viruses, HIV-1 and HIV-2. Closely related viruses (SIVs) are found in many species of non-human primates. Phylogenetic analyses indicate that cross-species transmission events have been quite frequent. Both HIV-1 and HIV-2 appear to have resulted from multiple transfers of lentiviruses naturally infecting other primates; the source of HIV-2 appears to have been sooty mangabeys, whereas for HIV-1 the source may have been chimpanzees. Phylogenetic analyses also provide evidence that recombination has occurred between divergent viruses in vivo. Evolutionary trees based on various regions of the viral genome generally have consistent branching orders. However, some isolates fall into significantly different phylogenetic positions, indicating that their genomes are mosaics of sequences with different evolutionary histories. This implies that co-infection with highly divergent viral strains can occur in HIV-infected humans and SIV-infected primates; this could lead to the generation of hybrid genomes with significantly altered biological properties, and also has important implications for HIV vaccine development programmes.

We determined the seroepizootiology of Helicobacter pylori infection in rhesus monkeys. Plasma was obtained from 196 animals (age range, 1 to 22 years) that were housed in social environments, either in indoor gang cages, in outdoor corrals, or in free-ranging forested conditions. Plasma immunoglobulin G levels were determined with a specific enzyme-linked immunosorbent assay, and the cutoff immunoglobulin G value for H. pylori seropositivity was determined from a study of 25 monkeys whose infection status was assessed by light microscopy and culture. One-year-old animals of both genders in all housing conditions had the lowest rate of positivity (60% in monkeys 1 year old versus 81% in monkeys 2 to 10 years old, P = 0.026). In addition, females tended to have higher rates of positivity than males. Seroconversion during a 1-year observation period occurred in 7 (28%) of 25 seronegative animals. Seroreversion occurred in 3 (4%) of the 78 positive animals; all 3 of these animals had received antimicrobial agents during the year. These observations demonstrate that the epizootiology of H. pylori infection in rhesus monkeys may serve as a model for human infection.

The importance of venereal modes of B virus (cercopithecine herpesvirus 1) transmission was evaluated in 49 rhesus monkeys tested at necropsy. Antibodies to B virus were demonstrated in 19 monkeys, but no active viral shedding was detected in mucosal swabs collected at death. The polymerase chain reaction demonstrated presence of the ICP 18.5 (UL28) gene of B virus in neuronal tissues of 15 monkeys presumed to be latently infected, including 12.8% of trigeminal and 22.9% of lumbosacral ganglia pools. Two monkeys tested positive at both sites. Breeding history was predictive of B virus seropositivity (odds ratio, 1.64; 95% confidence interval, 1.21-2.23; P < .05). The population attributable risk of B virus seropositivity due to breeding was 22.7%, similar to the proportion of monkeys with B virus DNA in neuronal tissues subserving the genital region. Sexual contact is a significant, but not predominant, mode of B virus transmission between monkeys.

Cercopithecine herpesvirus 1 (B virus), enzootic among monkeys of the genus Macaca, causes minimal morbidity in its natural host. In contrast, human B-virus infection presents as rapidly ascending encephalomyelitis with a fatality rate of approximately 70%. This infection remains an uncommon result of macaque-related injuries, although the increase in the use of macaques for research on simian retrovirus infection and hepatitis has expanded the number of opportunities for human exposure. In response to this situation, Emory University and the Centers for Disease Control and Prevention jointly sponsored a B Virus Working Group to formulate a rational approach to the detection and management of human B-virus infection. The resulting guidelines are presented herein and are based upon information from published cases, unpublished cases managed by working-group members, knowledge of the behavior of herpes simplex virus, and--in the absence of hard data--the collective judgment of the group. Although consensus among the co-authors existed on the major points covered by these guidelines, opinions varied widely regarding specific recommendations.

The epizootiologic properties of Herpesvirus simiae (B virus) were studied in singly housed macaques (Macaca mulatta and M. fascicularis) in a biomedical vivarium to determine whether commonly encountered environments and procedures such as quarantine, breeding, Caesarean section, parturition, and social stress induced virus shedding and transmission. Macaques were tested serologically and for infectious virus. Oral, conjunctival, and vaginal swab samples were obtained repeatedly. Virus excretion was not detected during a 7-week quarantine of 32 newly acquired, singly housed animals tested every other week for 6 weeks, and none of 19 seronegative animals from this group seroconverted during 7 weeks in quarantine. No virus shedding was detected in 16 seropositive animals tested weekly for 3 weeks after Caesarean section or normal parturition or in 11 seropositive animals following introduction of new males to animals rooms. One animal seroconverted after repeated breeding of seropositive animals to seronegative partners. Fifty-three singly housed offspring remained seronegative for up to 10 years, even if born to seropositive dams, and only 1 of 86 singly housed animals less than 7 years old was seropositive. These results suggest that shedding of B virus from seropositive macaques is uncommon, when subjected to common laboratory procedures or environments, and that transmission is rare in singly housed animals. These results may be useful in establishing B virus-free colonies of macaques.

A seroepidemiological study of arboviruses infecting 115 wild toque macaques (Macaca sinica) at Polonnaruwa, Sri Lanka showed a high prevalence of antibodies to dengue and Lumbo viruses. There was low seroprevalence of Chandipura (2/115) and Batai (1/115) virus antibodies, but no seropositivity to Chikungunya or Sindbis. There was no serological evidence of infection by Japanese encephalitis (JE) virus in spite of large human epidemics in the study area, indicating that toque macaques are unlikely to be an epidemiologically relevant host in the maintenance cycle of JE virus.

A small cluster of dysenteric illness, due to Shigella flexneri, was identified among technical assistants of a primate research unit. All of the affected individuals had been in regular contact with a colony of cynomolgus macaque monkeys, one of which was known to have suffered from acute haemorrhagic colitis in the preceding few weeks. Four monkeys were found to be excreting S. flexneri bacilli of identical antigen type (1b) to that isolated from the human cases. Investigation of working practices revealed the potential for inadvertent faeco-oral spread and the need to improve existing control methods. We conclude that this small outbreak of shigellosis represents a primate-associated occupational zoonosis. The risk may not be fully appreciated by handlers or their doctors.

Three SIVMne-infected female pigtailed macaques (Macaca nemestrina) were mated with two SIV-negative males. The females exhibited signs of SAIDS and SIVMne was readily isolated from peripheral blood mononuclear cells (PBMC). Both males became infected with SIVMne, developed SAIDS, and died. This is the first documented case of the transmission of SIVMne between adult macaques housed together. Although transmission through scratching or biting cannot be ruled out, heterosexual transmission appears the most likely mode of SIVMne transmission in this study.

Neurotropic vaccine strains of African horsesickness (AHS) virus types 1 and 6 were implicated as the possible aetiological agents in 4 cases of encephalitis and uveochorioretinitis in laboratory workers accidentally exposed to the freeze-dried vaccine preparations of the virus. To date, AHS virus has not been known to infect man. To ascertain whether or not primates were susceptible to infection with AHS virus, vervet monkeys (Cercopithecus pygerythrus) were inoculated, either transnasally or intraconjunctivally, with vaccine strains of AHS virus types 1 and 6. The course of infection was monitored using parameters such as behavioural changes, febrile reaction, cerebrospinal fluid pleocytosis, serology, magnetic resonance imaging and autopsy. Encephalitis, manifested by varying degrees of fever, behavioural changes and pleocytosis, but no chorioretinitis was detected in all 6 transnasally infected monkeys. This was confirmed by autopsy, where a meningo-encephalitis affecting the medial temporal lobe but no lesions in the eyes was demonstrated. Neither virus appeared to infect the animals after intraconjunctival inoculation. These findings support the theory that the patients were infected by the inhalation of freeze-dried vaccine preparations. The pathogenesis of the eye lesions, however, remains uncertain.

In Brazil simian malaria is widely spread, being frequent in the Amazon region (10% of primates infected) and even more in the forested coastal mountains of the Southeastern and Southern regions (35% and 18% infected, respectively), but absent in the semi-arid Northeast. Only two species of plasmodia have been found: the quartan-like Plasmodium brasilianum and the tertian-like P. simium, but the possible presence of other species is not excluded. P. brasilianum is found in all enzootic foci, but P. simium was detected only on the coast of the Southeastern and Southern regions, between paralles 20 degrees S and 30 degrees S. Nearly all hosts are monkeys (family Cebidae, 28 species harbouring plasmodia out of 46 examined), and very rarely marmosets or tamarins (family Callitrichidae, 1 especies out of 16). P. brasilianum was present in all infected species, P. simium in only two. The natural vector in the Southeastern and Southern regions was found to be Anopheles cruzi, but has not been conclusively identified in the Amazon. One natural, accidental human infection due to P. simium was observed. There is no evidence of the relation of simian to human malaria in the Southeastern and Southern regions, where human malaria was eradicated in spite of the high rates of monkeys infected, but in the Amazon recent serological studies by other workers, revealing high positivity for P. brasilianum/P. malariae antibodies in local indians, would suggest that among them malaria might possibly be regarded as a zoonosis.

A lactating primate, Callithrix jacchus, was infected experimentally with 600 mesocercariae of Alaria marcianae 10 days after parturition to determine if she would transmit the mesocercariae to her offspring. Her twin infants were examined 4 wk postinoculation and 16 mesocercariae were found in their tissues. The female was mated again and gave birth to a litter of triplets. She was not given additional mesocercariae. One infant died within hours of birth without suckling and was found negative for any stage of A. marcianae. The other 2 were allowed to nurse for 5 wk, examined and found to be infected with a total of 115 mesocercariae in various tissues, 1 metacercaria in the lungs, and 1 immature and 2 fully formed ovigerous adults in the small intestines. The female was examined at the same time and 246 mesocercariae were recovered. No other stage was found. Histological examination of her mammary glands revealed numerous mesocercariae in the milk-laden alveoli.

A strain of Plasmodium brasilianum was isolated from a naturally infected Saimiri monkey from Peru and subsequently passaged to 21 splenectomized Saimiri sciureus boliviensis monkeys. Nine of 12 attempts to transmit infection by sporozoite inoculation were successful with prepatent periods ranging from 23 to 41 days. Gametocytes were infective to Anopheles freeborni, Anopheles stephensi, Anopheles dirus, Anopheles maculatus, and Anopheles gambiae mosquitoes. The strain demonstrated a high level of resistance to cure with chloroquine.

The seroprevalence of antibodies to simian immunodeficiency virus (SIVsmm) and simian T-cell leukemia virus type I (STLV-I) in a captive breeding colony of sooty mangabey monkeys was determined, and infection by SIVsmm was confirmed in all cases by virus isolation. Among 138 animals tested, 57 and 33% were infected with SIVsmm and STLV-I, respectively. While the proportion of female mangabeys (66%) differed significantly (P less than 0.01) from the proportion of male mangabeys (42%) infected with SIVsmm, the proportions of males and females infected with STLV-I were similar, suggesting independent transmission of the two viruses. Among mangabeys less than 1 year old, none were infected with STLV-I and only five of 27 mangabeys, all of which were at least 6 months old when first tested, were infected with SIVsmm. The data document that natural infection of sooty mangabey monkeys with SIVsmm or in association with STLV-I infection does not result in increased disease or mortality, and that transmission of both SIVsmm and STLV-I appears to occur primarily through sexual activity.

The virulence of three isolates of simian immunodeficiency virus from African green monkeys (SIVagm) was studied in rhesus and pigtailed macaques. None of 15 rhesus monkeys and one of four pigtailed monkeys died from infection during the time they were studied (up to 33 months). SIVagm was only isolated from rhesus monkeys for up to 2 months after inoculation. However, when these animals were secondarily infected with Simian acquired immunodeficiency syndrome retrovirus type 1 (SRV-1), SIVagm was activated and isolated. Dual infection caused increased mortality.

The effect of temperature on the ability of Aedes aegypti to transmit dengue (DEN) 2 virus to rhesus monkeys was assessed as a possible explanation for the seasonal variation in the incidence of dengue hemorrhagic fever in Bangkok, Thailand. In two laboratory experiments, a Bangkok strain of Ae. aegypti was allowed to feed upon viremic monkeys infected with DEN-2 virus. Blood-engorged mosquitoes were separated into two groups and retained at constant temperatures. Virus infection and transmission rates were determined for Ae. aegypti at intervals ranging from 4 to 7 days during a 25-day incubation period. Results of the first experiment for mosquitoes infected with a low dose of DEN-2 virus and maintained at 20, 24, 26, and 30 degrees C, indicated that the infection rate ranged from 25% to 75% depending on the incubation period. However, DEN-2 virus was transmitted to monkeys only by Ae. aegypti retained at 30 degrees C for 25 days. In the second experiment, the infection rate for Ae. aegypti that ingested a higher viral dose, and incubated at 26, 30, 32, and 35 degrees C ranged from 67% to 95%. DEN-2 virus was transmitted to monkeys only by mosquitoes maintained at greater than or equal to 30 degrees C. The extrinsic incubation period was 12 days for mosquitoes at 30 degrees C, and was reduced to 7 days for mosquitoes incubated at 32 degrees C and 35 degrees C. These results imply that temperature-induced variations in the vector efficiency of Ae. aegypti may be a significant determinant in the annual cyclic pattern of dengue hemorrhagic fever epidemics in Bangkok.

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.

Eight different anophelines--Anopheles freeborni, An. maculatus, An. dirus, An. stephensi, An. atroparvus, An. sundaicus, An. quadrimaculatus, and An. albimanus--were shown to be susceptible to infection with a strain of Plasmodium gonderi from the drill. Mandrillus leucophaeus. Transmission was obtained via the bites of An. freeborni, An. maculatus, An. stephensi, and An. dirus mosquitoes to Macaca mulatta. Prepatent periods in Macaca mulatta monkeys following sporozoite inoculation ranged from 7 to 15 days with a median of 12.5 days. Relapses from fixed-tissue stages following treatment with chloroquine or quinine sulfate were not demonstrated.

We report here a family with three pathologically confirmed cases of Creutzfeldt-Jakob disease in three siblings and with transmission of one case to the squirrel monkey. This family, originating from the South-East of England, settled in France in 1870. Eight members of the family, distributed in three generations, were affected by the disease at the same age (about 50), with similar symptoms and length of evolution. Two cases were confirmed at post-mortem and one case by cerebral biopsy. The genealogic inquiry dealth with 46 members of 5 generations. All the affected members, six men and two women, belonged to the three older generations which were comprised of 15 individuals. All had lived in close relationship in a limited area of the north of Ardennas. The possible mechanisms of dominant inheritance or cross infection are discussed.

A 2.5-year epidemiologic study of a breeding group of rhesus monkeys (Macaca mulatta), which is a focus of endemic simian acquired immunodeficiency syndrome (SAIDS), demonstrated a strong association between the occurrence of SAIDS and infection with a type D retrovirus, SAIDS retrovirus serotype 1 (SRV-1). Of 23 healthy "tracer" juvenile rhesus monkeys, 19 (83%) died with SAIDS within 9 months of introduction into the resident SAIDS-endemic population. In contrast, 21 healthy "sentinel" juvenile rhesus monkeys placed in the same outdoor enclosure but denied physical contact with the SAIDS-affected group by a 10-foot-wide "buffer zone" remained free of SRV-1, SRV-1 antibody, and disease for 2.5 years. The SAIDS-specific mortality rate was significantly higher in juveniles than in adults. In repeated serologic testing, the overall prevalence of SRV-1 antibody ranged from 68 to 85%. Antibody prevalence increased with age. Seroconversion was found to be a poor indicator of infection rate, as approximately 50% of virus-positive juvenile monkeys had no antibody detectable by enzyme-linked immunosorbent assay. Repeated viral isolations from all animals revealed 1) SRV-1 viremia with clinical SAIDS; 2) persistent viremia and viral shedding in apparently healthy animals; 3) transient viremia and clinical recovery; 4) intermittent viremia, suggesting activation of latent infections; and 5) viremia in a 1-day-old infant, suggesting transplacental transmission. The prevalence of SRV-1 antibody in SAIDS-free breeding groups of rhesus monkeys was 4%. The seroprevalence of antibodies against human T-cell leukemia virus type 1 (HTLV-1), human immunodeficiency virus (HIV), and simian immunodeficiency virus (SIV; formerly STLV-III) was uniformly low or absent in both SAIDS-free and SAIDS-affected groups of rhesus monkeys, demonstrating that these retroviruses are not etiologically linked to SAIDS at the California Primate Research Center.

Tamarins (Saguinus mystax and Saguinus labiatus) were experimentally infected with two strains of measles virus. One of the strains (JM) spread readily among the animals with a high fatality rate. The second strain (Edmonston) appeared to be less pathogenic and less transmissible than strain JM. Aerosol was considered the most probable mode of infection.

Studies of B virus (Herpesvirus simiae) antibody in several species of macaque lead to the following generalizations. Newborn monkeys are not infected with B virus, even when born of seropositive mothers. Young monkeys remain uninfected until they become adults. The majority of adults develop B virus antibody unless their physical contact with seropositive adults is restricted. These observations are consistent with sexual transmission of B virus and classification of the disease in monkeys as venereal. However, infection at oral and dermal sites also occurs and may play a part in monkey-to-monkey transmission. Epizootics of B virus occurred during early attempts to start B virus-free breeding colonies. They appeared to originate from reactivated latent B virus in adult monkeys which had only low titres of antibody. The stress produced when groups of adult strangers were assembled to form breeding colonies was the most effective known inducer of latent B virus. Total exclusion of animals with any trace of antibody has enabled the establishment of new breeding colonies which are free from B virus.

The existence of naturally acquired leprosy in a second sooty mangabey monkey has been documented. The disease has the clinical and histopathological characteristics of subpolar lepromatous leprosy (LLs), and microbiological studies thus far confirm the etiologic agent as Mycobacterium leprae. This mangabey had been housed in direct contact with the first mangabey in which naturally acquired leprosy was diagnosed in 1979. Clinical symptoms appeared in the second mangabey in 1986, almost 7 years after the appearance of skin lesions in the first monkey. It is likely that the second mangabey contracted leprosy from the first mangabey or that both animals contracted the disease by contact with an unknown common third source. This is the only known possible natural transmission of leprosy from monkey to monkey, and suggests that a potential zoonosis exists in wild monkeys that may serve as a reservoir for the disease in areas where human leprosy is endemic.

Brain homogenates (10% w/v) from five of seven kuru patients inoculated intracerebrally (i.c., 0.1 ml) into marmosets (Saguinus sp.) induced a rapidly progressive CNS disease 26, 31, 36, 76 and 94 months postinoculation. Serial marmoset passages of kuru were accomplished by i.c. inoculation of neonatal marmosets with brain homogenates from marmosets with experimentally induced kuru. The incubation periods ranged from 1.5 to 11 months (average 7.3) in 19 animals, 20-25 months in four animals and greater than 26 months in two animals. Symptoms and brain lesions of the induced disease were compatible with kuru as observed in humans and other nonhuman primates. Creutzfeldt-Jakob disease (CJD) has been induced by i.c. inoculation of marmosets with brain homogenates from two of four human CJD patients with incubation periods of 43 and 54 months and is in serial passage.

Leukemia virus transmission was studied during an outbreak of leukemia among the baboons of the Sukhumi monkey colony. First, the possibility of "vertical" transmission of the virus was examined, as the Papio stock in Sukhumi was genetically homogeneous. "Vertical" transmission of the virus from a common ancestor seems unlikely, since cases of leukemia were registered in animals descending from different families. However, there were cases of innate leukemia, when babies born from leukemic parents displayed pronounced signs of leukemia immediately after birth. "Horizontal" transmission of the virus also seems indisputable, because special experiments have shown that imported baboons, even of other species, caged together with leukemic animals, may develop leukemia due to close contact. It was established earlier that the leukemia virus was excreted with urine. Kidneys, lungs, and salivary glands are the possible routes of infection. Thus, the present report aknowledges the possibility of both "horizontal" and "vertical" transmission of leukemia oncornaviruses in primates.

Herpesvirus saimiri was naturally transmitted from squirrel monkeys excreting the virus to one of two owl monkeys housed in the same cage. The owl monkey became infected approximately three months after contact was initiated. H. saimiri was consistently isolated from the peripheral lymphocytes until this animal died eight months later. During this period the owl monkey developed specific antibody to H. saimiri to a maximal neutralization index of 5.5 logs. The other monkey remained uninfected for an ovservation period of one year. The documentation of this horizontal transmission of H. saimiri infection from squirrel monkeys to an owl monkey suggests that owl monkeys developing spontaneous malignant lymphomas associated with H. saimiri infection may also have acquired the infection in this manner.

In the past 5 years 17 human cases of monkeypox with 4 deaths were reported in African countries. The source and the mechanism of transmission of the infection are unknown. One of the possible modes of human infection could be through monkey meat used for food. The paper presents the results of the study of susceptibility of 4 species of laboratory animals to monkeypox virus given orally. Adult rabbits, guinea pigs, and hamsters were found to be resistant. Ten-day-old rabbits and 8-, 10- and 12-day-old mice developed generalized infection with eruptions and high lethality. The infection was transmitted to uninfected rabbits of the same litter, apparently by air-borne droplet mode. The obtained model of generalized monkeypox infection after per os administration of the virus and the fact of air-borne droplet transmission of infection may serve as indirect evidence of the possibility of transmission of the infection by this mode in nature.

Antibodies which probably indicate infection with human T-cell leukaemia virus type I (HTLV-I) were determined in three species of non-human primates from several localities. A significant prevalence among chacma baboons and vervet monkeys was confirmed. According to sero-epidemiological evidence that HTLV-I infection is predominantly sexually transmitted between adult animals; comparison of prevalence rates between localities or species should therefore take sexual maturity into account. It appears unlikely that transmission from non-human primates to humans is frequent.