The effect of suppression of fever on viral levels in nasal washes of ferrets infected with either of two clones (7a, virulent; 64d, attenuated) of the recombinant influenza virus A/Puerto Rico/8/34-A/England/939/69 (H3N2) was studied. The febrile response was reduced by shaving the ferrets or by treating them with sodium salicylate, which had no noticeable effect on the inflammatory response. For both clones, significantly more virus was shed in the nasal washes of ferrets whose febrile response was suppressed, and the viral levels decreased less rapidly than in untreated ferrets or in those in which the treatments were ineffective.
SUMMARYThe distribution of four strains of influenza virus [A/PR/8/34 (HON 1) and clone 64d (attenuated for ferrets) and clones 64c and 7a (virulent for ferrets) of the recombinant virus A/PR/8/34-A/England/939/69 (H3N2)] in the lower respiratory tract (trachea, bronchi and the hilar, intermediate and outer alveolar zones of the lung) of ferrets was monitored daily for 4 days after intranasal inoculation. On day 1, some animals had high virus titres in all the tissues but in other animals virus was undetectable, irrespective of the virus strain. Two days after inoculation increase of virus contents of all tissues tended to be restricted. On days 3 and 4, the virulent clones (64c and 7a), in contrast to the attenuated strains (A/PR/8/34 and clone 64d), consistently infected the lower respiratory tissues. However, for all infected animals the virus contents of the hilar zones of the lungs were higher than those in the intermediate zones, while the alveolar zones were relatively free from virus. Quantitative estimations of the mild histological damage occurring in the lower respiratory tract 3 to 6 days after inoculation also indicated that bronchial and bronchiolar tissue were more susceptible to influenza virus than alveolar tissue and that clones 64c and 7a produced more damage than the other two strains. In agreement with the relative viral contents of clones 64c and 7a in the bronchi and in the hilar and intermediate zones of the lung, clone 64c produced more damage than clone 7a in the bronchi and less in the bronchioles of the lung parenchyma.
Pregnant ferrets were inoculated intra-cardially on day 30 of gestation with influenza virus. The animals were sacrificed on days 5 to 11 after inoculation and the products of conception including the uterus were examined virologically and histopathologically. The results indicate that the initial site of infection of the conceptus is the haemophagous organ and that spread occurs from this site to the endometrium, placental labyrinth and fetus. Lesions in the fetus are confined to the liver and respiratory tract. In the liver they may represent either a viral hepatitis or a secondary response to placental damage resulting in the stimulation of erythropoiesis. In the respiratory tract they first occur in the nasal sinuses and upper airways suggesting that infection is via the amniotic fluid rather than via the blood stream. The relevance of these findings to human pregnancy is discussed.
We present two cases of acute r enal failure associated wi t h a microangiopathic haemol ytic anaemia followin g pneu mococcal infections. In both children t here was evidence o.f red cell T-poly-egglutinability (bsing msn i f es t initially as discrspant ABO blood group ing) . In one child pneumococci were i so l at e d from the blood whilst in the other there wee antigenic ev idence of a recent pneumococcal i nf ec t i on . Both ch ildren had a period of oliguric renal failure requiring dialysis. Prostaglandin metabolism was s hown to be normal in both children. Renal biopsy in one Case showed evidence of exposure of the T antigen on the re nal glomeruli, tubules and fed cell casts. Pneumococci are known to produce the enzyme neuraminidase which has been implicated in Tactivstion. We suggest that T-activation following pneumococcal infection should be included In the spectrum of the Haemolytic Uraemic Syndrome. in all l'/'<4>S. It 19~tl'at in tl'l>o SIIIS the lU1@;3 are rot cnly free fran 1nIlaImntory changes, tut also """ s1g19 of prev100s eventa causI~peteclllal ha
SUMMARYUsing fluorescent antibody techniques, a semi-quantitative survey has been made of the distribution of influenza virus antigen in the trachea, main bronchi, and three zones (hilar, intermediate and alveolar) of all four lung lobes of ferrets following intranasal inoculation of a virulent clone (7a) of the recombinant influenza virus A/PR/8/34-A/England/939/69 (H3N2). The results confirm the indications from our previous quantitative surveys of infectious virus and histological damage in these areas, namely that infection is confined largely to airway epithelium and is rare in the alveoli. Furthermore, in the lung zones, viral antigen resided mainly in the bronchial rather than bronchiolar epithelium. In attempts to identify the reasons for lack of alveolar involvement organ cultures of alveolar tissue, from which all major airways had been removed, produced levels of virus similar to cultures of bronchus and trachea and the hilar and intermediate lung zones which contain airway and alveolar tissue. Hence, the lack of alveolar infection in vivo must be due to factors which prevent virus attack of susceptible alveolar cells. However, these organ culture experiments showed that a contributing factor could be very poor release of virus from any alveolar cells that do become infected. In contrast, although cultures of bronchi produced less virus than those of nasal turbinates (the most susceptible tissue in vivo) they released a high proportion of their yield and this ease of release may contribute to spread of infection in vivo.
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