In the context of this study the ethnic origin of the patients revealed no noteworthy difference in the clinical reaction to the parasite; neither did age or sex of the patients. Any minor differences whcih appeared in length of history before seeking treatment and frequency of repeat attacks were more a reflection of the cultural pattern of response to illness (i.e. resort to traditional medicines) and the distance between the patient's home and the doctor rather than any altered response on the part of the host to the parasite. However, the fact that about 35 per cent of all the episodes had a history of eight or more days (about 10 per cent more than 30 days) suggest that more "malaria consciousness" is called for in what is after all an endemic malaria area. The value (and necessity) of repeated examination of the blood to detect the parasite is confirmed but it is also encouraging to note that in 84% of cases a single careful examination of the blood revealed the parasite. Since in 49% of our malaria episodes the patient was afebrile when the parasite was discovered, it is obvious that in outpatient practice especially blood should be examined when the patient presents for treatment, irrespective of the presence or absence of pyrexia. As always, a prerequisite to the diagnosis of malaria is an awareness of its possible presence.
A study of 1,437 unselected febrile patients in rural Malaysia yielded a diagnosis of leptospirosis in 86 (6.0%). The clinical syndrome was mild to moderate in all cases, jaundice was observed in only 2 (2.3%) and no deaths were documented. The diagnosis was not clinically obvious in most cases, and it is apparent that many infections must be going unnoticed at present.
One hundred and fourteen Rickettsia tsutsugamushi isolates, recovered from febrile patients in central Peninsular Malaysia, were antigenically analyzed by direct immunofluorescence using eight prototype strains. Twenty-nine antigenic types were detected. The TA763, TA716, Karp and TA686 strains were the most common and occurred singly or in combination with each other or other strains in 86% of the isolates.
In 1977 and 1978 selected in-patients at the Tegalyoso Hospital, Klaten, Indonesia who had recent onsets of acute fever were serologically studied for evidence for alphavirus and flavivirus infections. A brief clinical history was taken and a check list of signs and symptoms was completed on admission. Acute and convalescent phase sera from 30 patients who showed evidence that a flavivirus had caused their illnesses were tested for neutralizing antibodies to several flaviviruses which occur in South-east Asia. Paired sera from seven patients demonstrated a fourfold rise in antibody titre from acute to convalescent phase. The most common clinical manifestations observed in this series of patients included high fever, malaise, stomach ache, dizziness and anorexia. None of the seven patients had headache or rash despite the fact that headache and rash had been associated with two of the three previously studied. The onsets of illness clustered toward the end of the rainy season when populations of Aedes aegypti, a probable vector in Malaysia, were most abundant.
Patients attending a referral Skin Clinic were studied to identify the spectrum of drug eruptions and the offending drugs. There were 51 patients with an incidence of five per thousand and equal sex incidence. Though the pattern of eruption was broadly similar to other reports, unusual reactions were observed. In addition to the skin manifestation, fever and lymphadenopathy were present in most patients. Raised erythrocyte sedimentation rate and eosinopoenia were commonly observed. Clinical acumen and the list of drugs ingested are still the best clues to the diagnosis ofdrug eruption.
Study site: Skin clinic, University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
Malaria is still a very real threat to health in S.E. Asia including Malaysia. While there has been a dramatic fall in the number of cases and also the number of deaths from the disease in Malaysia cases are still occurring and there has actually been a rise in the number of deaths in the past year. Parts of Perak and the East Coast states are still high risk areas in Peninsular Malaysia. While 95 percent of the population of Peninsular Malaysia is now malaria-free there has also been a concomitant loss of herd immunity which means that if a non-immune person contracts falciparum malaria he stands a greater chance of a fatal outcome. Doctors and other health personnel should be more malaria conscious and make a practice of making blood films of all cases of fever. This is especially important in the rural areas and Estate Hospital Assistants must be encouraged to look for malaria parasites in their fever patients. The younger generation of EHAs have little experience of malaria and a definite policy of education to bring them up to date in antimalarial work and microscopic detection of the parasite should be under taken by the industry. Some problems of chemotherapy and drug resistance are discussed.
Brugia malayi and Wuchereria bancrofti infections cause lymphatic filariasis in Malaysia. About 2.5 million people live in endemic areas of filariasis, of whom 5% have microfilaraemia and probably twice as many are infected. There is a wide clinical spectrum of response to the infection. While some have asymptomatic microfilaraemia, others have episodic attacks of fever, lymphadenitis, retrograde lymphangitis and lymphoedema. Elephantiasis is a late complication. Tropical pulmonary eosinophilia and other forms of occult filariasis are due to hyper allergic reactions to microfilarial antigens. Parasitological and serological tests aid in confirming the clinical diagnosis. The drug of choice is diethylcarbamazine citrate.
The pattern of phage types of 2553 strains of Salmonella typhi isolated over the 10-year period 1970-9 was studied. During the period 29 different phage types were encountered, not including the categories of 'untypable strains', 'degraded Vi-strains' and Vi negative strains. For the period as a whole, the commonest phage types encountered were A (20.9%), E1 (14.8%), D1 (10.3%), degraded Vi positive strains (10.3%), untypable Vi strains (7.3%), C4 (7.1%), D2 (4.4%), E2 (3.9%) and type 25 (2.6%). There were phage types which appeared in the early years of the period and then disappeared (types B2, D9 and D1-N). Others only made their appearance in recent years (K1 and 53). Notable differences were also seen in the predilection of some phage types for certain geographical areas.
The diagnostic value of the Widal test was assessed in an endemic area. The test was done on 300 normal individuals, 297 non-typhoidal fevers and 275 bacteriologically proven cases of typhoid. Of 300 normal individuals, 2% had an H agglutinin titre of 1/160 and 5% had an O agglutinin titre of 1/160. On the basis of these criteria a significant H and/or O agglutinin titre of 1/320 or more was observed in 93-97% of typhoid cases and in only 3% of patients with non-typhoidal fever. Of the sera from typhoid cases which gave a significant Widal reaction, the majority (79.9%) showed increases in both H and O agglutinins and 51 of 234 (21.8%) of these sera were collected in the first week of illness. The significance and implications of these findings are discussed.
We studied 1,629 febrile patients from a rural area of Malaysia, and made a laboratory diagnosis in 1,025 (62.9%) cases. Scrub typhus was the most frequent diagnosis (19.3% of all illnesses) followed by typhoid and paratyphoid (7.4%); flavivirus infection (7.0%); leptospirosis (6.8%); and malaria (6.2%). The hospital mortality was very low (0.5% of all febrile patients). The high prevalence of scrub typhus in oil palm laborers (46.8% of all febrile illnesses in that group) was confirmed. In rural Malaysia, therapy with chloramphenicol or a tetracycline would be appropriate for undiagnosed patients in whom malaria has been excluded. Failure to respond to tetracycline within 48 hours would usually suggest a diagnosis of typhoid, and indicate the need for a change in therapy.
A seroepidemiological survey of 837 people and 383 febrile patients was performed in rural areas of Sabah. We determined that the rickettsial diseases scrub typhus and endemic typhus were uncommon causes of febrile illness, as was tick typhus, except in forest dwelling peoples. The rate of occurrence of SFGR specific antibody was 16.5% among 412 forest dwellers, indicating that tick typhus may be a frequent cause of illness in this population.
A case of haemorrhagic fever with renal syndrome that originated in Malaysia is reported. The patient presented with clinical symptoms which were not typical of the disease as seen in endemic regions. Renal involvement, which is characteristic of haemorrhagic fever with renal syndrome, was mild, and the predominant symptom was a persistently marked elevation of serum transaminase levels that was suggestive of hepatitis. Liver involvement has not been described in the Asian form of haemorrhagic fever with renal syndrome. The patient developed a petechial skin rash and had severe thrombocytopenia. Serological confirmation of the diagnosis of haemorrhagic fever with renal syndrome was obtained by the demonstration of significant antibody rises to hantaviruses in the patient's acute- and convalescent-phase sera.
Matched MeSH terms: Hemorrhagic Fever with Renal Syndrome/complications*; Hemorrhagic Fever with Renal Syndrome/diagnosis
Haemorrhagic fever with renal syndrome (HFRS) is caused by a group of RNA viruses within the family of Bunyaviridae known as hantaviruses. The classical, severe form of HFRS is characterized by fever, headache, abdominal and lumbar pain, proteinuria, haemorrhagic phenomena, shock and renal failure. The disease is associated with the prototype Hantaan virus and occurs in rural areas of Korea and China with Apodemus mice as reservoir hosts. A clinically less severe form of HFRS, which is caused by Seoul virus, occurs in urban areas with the house rat Rattus novegicus as the main reservoir host. The disease in nonendemic areas may be atypical and patients with symptoms the hepatitis and minimal renal involvement have been observed in Malaysia. Outbreaks of HFRS in humans involving infected laboratory rat colonies have occurred in several medical centres in various countries. Hantaviruses cause a chronic, asymptomatic infection in rodents which excrete the virus in their lungs, saliva and urine. Man becomes infected mainly by inhalation of infected droplets from healthy rodent carriers. Seroepidemiological studies using mainly the indirect immunoflourescent antibody test of sera from humans and rats showed that hantaviruses have a worldwide distribution.
Matched MeSH terms: Hemorrhagic Fever with Renal Syndrome/epidemiology; Hemorrhagic Fever with Renal Syndrome/transmission*