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A 27-year-old woman presented to a hospital with symptoms resembling pyelonephritis; respiratory distress did not develop until nearly a day after admission and she subsequently died. The Unexplained Deaths and Critical Illnesses Project of the Centers for Disease Control and Prevention confirmed Sin Nombre virus infection by the results of serological testing and sequencing of the viral genome; staining of Sin Nombre virus antigen in the pulmonary capillaries was relatively weak.

Influenza viruses are responsible for acute febrile respiratory disease. When deaths occur, definitive diagnosis requires viral isolation because no characteristic viral inclusions are seen. We examined the distribution of influenza A virus in tissues from 8 patients with fatal infection using 2 immunohistochemical assays (monoclonal antibodies to nucleoprotein [NP] and hemagglutinin [HA]) and 2 in situ hybridization (ISH) assays (digoxigenin-labeled probes that hybridized to HA and NP genes). Five patients had prominent bronchitis; by immunohistochemical assay, influenza A staining was present focally in the epithelium of larger bronchi (intact and detached necrotic cells) and in rare interstitial cells. The anti-NP antibody stained primarily cell nuclei, and the anti-HA antibody stained mainly the cytoplasm. In 4 of these cases, nucleic acids (ISH) were identified in the same areas. Three patients had lymphohistiocytic alveolitis and showed no immunohistochemical or ISH staining. Both techniques were useful for detection of influenza virus antigens and nucleic acids in formalin-fixed paraffin-embedded tissues and can enable further understanding of fatal influenza A virus infections in humans.

During 10-19 March 1999, 11 workers in 1 of 2 Singaporean abattoirs developed Nipah-virus associated encephalitis or pneumonia, resulting in 1 fatality. A case-control study was conducted to determine occupational risk factors for infection. Case patients were abattoir A workers who had anti-Nipah IgM antibodies; control subjects were randomly selected abattoir A workers who tested negative for anti-Nipah IgM. All 13 case patients versus 26 (63%) of 41 control subjects reported contact with live pigs (P=.01). Swine importation from Malaysian states concurrently experiencing a Nipah virus outbreak was banned on 3 March 1999; on 19 March 1999, importation of Malaysian pigs was banned, and abattoirs were closed. No unusual illnesses among pigs processed during February-March were reported. Contact with live pigs appeared to be the most important risk factor for human Nipah virus infection. Direct contact with live, potentially infected pigs should be minimized to prevent transmission of this potentially fatal zoonosis to humans.

After the large-scale outbreak of Ebola hemorrhagic fever (EHF) in Bandundu region, Democratic Republic of the Congo, a program was developed to help detect and prevent future outbreaks of EHF in the region. The long-term surveillance and prevention strategy is based on early recognition by physicians, immediate initiation of enhanced barrier-nursing practices, and the use of an immunohistochemical diagnostic test performed on formalin-fixed skin specimens of patients who die of suspected viral hemorrhagic fever. The program was implemented in September 1995 during a 4-day workshop with 28 local physicians representing 17 of 22 health zones in the region. Specimen collection kits were distributed to clinics in participating health zones, and a follow-up evaluation was conducted after 6 months. The use of a formalin-fixed skin specimen for laboratory confirmation of EHF can provide an appropriate method for EHF surveillance when linked with physician training, use of viral hemorrhagic fever isolation precautions, and follow-up investigation.

A patient with undiagnosed Ebola (EBO) hemorrhagic fever (EHF) was transferred from Kikwit to a private clinic in Kinshasa, Democratic Republic of the Congo. A diagnosis of EHF was suspected on clinical grounds and was confirmed by detection of EBO virus-specific IgM and IgG in serum of the patient. During the course of the disease, although she had no known predisposing factors, the patient developed a periorbital mucormycosis abscess on eyelid tissue that was biopsied during surgical drainage; the abscess was histologically confirmed. Presence of EBO antigen was also detected by specific immunohistochemistry on the biopsied tissue. The patient survived the EBO infection but had severe sequelae associated with the mucormycosis. Standard barrier-nursing precautions were taken upon admission and upgraded when EHF was suspected; there was no secondary transmission of the disease.

Laboratory diagnosis of Ebola hemorrhagic fever (EHF) is currently performed by virus isolation and serology and can be done only in a few high-containment laboratories worldwide. In 1995, during the EHF outbreak in the Democratic Republic of Congo, the possibility of using immunohistochemistry (IHC) testing of formalin-fixed postmortem skin specimens was investigated as an alternative diagnostic method for EHF. Fourteen of 19 cases of suspected EHF met the surveillance definition for EHF and were positive by IHC. IHC, serologic, and virus isolation results were concordant for all EHF and non-EHF cases. IHC and electron microscopic examination showed that endothelial cells, mononuclear phagocytes, and hepatocytes are main targets of infection, and IHC showed an association of cellular damage with viral infection. The finding of abundant viral antigens and particles in the skin of EHF patients suggests an epidemiologic role for contact transmission. IHC testing of formalin-fixed skin specimens is a safe, sensitive, and specific method for laboratory diagnosis of EHF and should be useful for EHF surveillance and prevention.

In October 1995, epidemic "hemorrhagic fever," without jaundice or renal manifestations, was reported in rural Nicaragua following heavy flooding; 2259 residents were evaluated for nonmalarial febrile illnesses (cumulative incidence, 6.1%) and 15 (0.7%) died with pulmonary hemorrhage. A case-control study found that case-patients were more likely than controls to have ever walked in creeks (matched odds ratio [MOR], 15.0; 95% confidence interval [CI], 1.7-132.3), have household rodents (MOR, 10.4; 95% CI, 1.1-97.1), or own dogs with titers >/=400 to Leptospira species (MOR, 23.4; 95% CI, 3.6-infinity). Twenty-six of 51 case-patients had serologic or postmortem evidence of acute leptospirosis. Leptospira species were isolated from case-patients and potential animal reservoirs. This leptospirosis epidemic likely resulted from exposure to flood waters contaminated by urine from infected animals, particularly dogs. Leptospirosis should be included in the differential diagnosis for nonmalarial febrile illness, particularly during periods of flooding or when pulmonary hemorrhage occurs.

Partitioning of assimilated carbon among sink organs is a critical factor that controls the rate and pattern of plant growth. Time-course measurements of plant and organ growth rates are useful for determining how regulation of carbon partitioning controls plant growth. Measuring growth rates over a 24 h period reveals the current pattern of carbon partitioning that can be used to predict growth rates of specific sinks. Comparison of growth rates among sinks under defined conditions can point out key factors that regulate partitioning of recently assimilated carbon among sinks. Internal control of carbon partitioning by developmental programmes regulates the timing and site of carbon distribution among developing parts, thereby establishing the adaptive traits of a species, cultivar or transgenic construct. Regulation of partitioning in response to environmental factors establishes or restores allometric growth among plant parts and functional balance between the supply and use of carbon. Environmental stress often restricts resource availability while successful acclimation sets in motion processes that restore the supply. A key mechanism contributing to regulation of carbon partitioning is an expression of genes that control activity of the enzymes which initiate sucrose metabolism at specific sites and stages of ontogeny.