Influenzal Pneumonia Research Articles

Mediastinal Cyst

The patient, a married woman, aged 35, had influenzal pneumonia in November, 1918, from which she felt she had never fully recovered. A thyroidectomy in April, 1920, was followed by pneumonia, the patient being confined to bed for seven weeks. Since then there has been continuous cough and copious expectoration of thick, foul sputum. Some morning temperature. Marked loss of weight and energy. X-ray examination, September 7, 1920, showed globular, non-pulsating mass (Fig. 1) 4½ inches in diameter attached to the upper mediastinal shadow and closely related to the left main bronchus, through which it probably drained. It lay behind the bifurcation of the trachea (Fig. 3) and displaced the esophagus 1½ inches to the right and backwards (Fig. 3) . The posterior wall of the shadow was about 1¼ inch from the posterior thoracic wall. An outline of the mass was transposed to an anatomical cross-section of the region. The relation of the shadow to the mediastinum, its partial drainage through the bronchus, and its even, globular, non-pulsating outline suggested cyst. Several attempts at aspiration were made, but without success. Finally, with the assistance of an improvised arrangement of two fluoroscopes at right angles, a small caliber needle 3½ inches long was inserted safely through the posterior wall. The needle point being found to be well within the mass, aspiration was attempted, but, owing to the thickness of the contents, met with only partial success. A small amount of air was injected which proved by its change of position when the patient assumed various postures that the contents of the mass was fluid or semi-fluid (Fig. 2). The surgeon followed up the needle, still in place, establishing partial drainage. Following this procedure there was complete cessation of cough and expectoration, and a rapid gain in weight and strength followed, with an improvement in general physical condition. The laboratory test, March 7, 1921, showed saprophytic organisms: no fetal parts. Subsequent Course Until October 13, 1925, when the patient was last seen, examinations were made from time to time. The empty cyst as shown in Figures 3 and 4 was readily visible and of only slightly diminished size. The distortion of the esophagus during these five years has remained practically unchanged (Fig. 3). The patient, who refuses further operation, remains in excellent health and has gained about fifty pounds in weight. There is no cough and no expectoration, but the tube is retained in position. Drainage is practically nil, the dressing applied once or twice daily showing only a stain and the odor is scarcely noticeable. An attempt to remove the tube about two years ago demonstrated its impracticability at that time by a return of the symptoms.

Anatomic Study of Rabbit Snuffles with Special Reference To Etiology, and Correlation with Experimental Pfeiffer Bacillus Pneumonia and Human Influenzal Pneumonia

Anatomic Study of Rabbit Snuffles with Special Reference To Etiology, and Correlation with Experimental Pfeiffer Bacillus Pneumonia and Human Influenzal Pneumonia

Observations on the inter-relations of pulmonary tuberculosis, influenza and pneumonia

Summary In their own homes the tuberculous suffered attacks of influenza at least as frequently as the population at large. The adult cases of pulmonary tuberculosis in residence at Barrasford Sanatorium and the Tuberculosis Wards at the City Hospital escaped the epidemics almost completely. The isolation of the first-named institution may have accounted for its immunity; on the other hand it is difficult to explain why the hospital patients got off practically “scot free” as 50 per cent, of the nursing and domestic staffs were affected during the 1918–19 epidemic. Post influenzal pseudo-tuberculosis and tuberculous pseudo-influenza caused considerable confusion in diagnosis. Acute influenzal pneumonia was found to be followed by pulmonary tuberculosis in a greater proportion of instances than was lobar pneumonia; the total number of cases, however, was small and there was no evidence that influenza proper was a serious factor in increasing the morbidity of tuberculosis. While 15·9 per cent, of the new sputum-positive cases registered between June 1, 1918, and June 30, 1920, ascribed their pulmonary tuberculosis to influenza it has to be borne in mind that at least 20 per cent, of the population at large suffered from an attack of influenza during the 1918–19 epidemic. Many of the definite cases suffered an aggravation of their disease as a result of an attack of influenza, and two patients with an artificial pneumothorax died of acute influenzal pneumonia. During and immediately after the 1918–19 epidemic the death returns revealed an increase in the number of deaths from pulmonary tuberculosis; this increase can, in part at least, be ascribed to influenza. Since then the death-rate from pulmonary tuberculosis has progressively declined and that of 1922 was the lowest ever recorded in the city.

AUTOSERUM TREATMENT OF PNEUMOCOCCUS MENINGITIS COMPLICATED BY SYPHILIS

Intraspinal injection of autoserum has recently been used with considerable success in the treatment of pneumococcus meningitis; 1 but references in the literature 2 warn against its use in cases complicated by syphilis, for fear of spreading this disease to the meninges. This caution seems to be founded on premature judgment, for the patient with syphilis who develops a secondary meningitis may be safely and wisely so treated by combining the autoserum with arsphenamin in the form of modified Swift-Ellis treatment. REPORT OF CASE History. —G. H. S., an American farmer, aged 22, married, entered the hospital, Feb. 22, 1920, complaining of headache, vomiting and fever. Two weeks before, he had had influenza complicated by influenzal pneumonia, but for three or four days had been up and around the house. Twenty-four hours before admission, he began to ache all over, and had a severe headache, high fever, rigidity of the

A CASE OF PROBABLE PARAFFIN-OIL TUMOR

In March, 1920, Mook and Wander 1 described for American literature, on the basis of a considerable series of cases, a foreign-body tumor of the arm, essentially a modification of the familiar paraffinoma, following the hypodermic administration of adulterated camphorated oil in which the olive oil of the pharmacopeial preparation was replaced by liquid petrolatum. The preparation apparently had been used in the treatment of influenzal pneumonia. Clinically the paraffin-oil tumor described by Mook and Wander consists of a brawny indurated and nodular infiltration of the arm having the histologicstructure of a granuloma in the inflammatory phase and of a paraffinoma in the quiescent or fibrous stage. CASE REPORT Clinical Appearance of Tumor.— The clinical appearance of the tumor in the case reported was typical of the inflammatory phase. Chains and nodules extended from the lesion in the larger part of the anterior and posterior surfaces of the left upper

The correlation of rabbit pneumonia and human influenzal pneumonia

In this paper I wish to report certain studies on pneumonia in rabbits and incidently to compare the lesions with the lesions in human influenzal pneumonia. An epidemic of rabbit influenza occurred among the laboratory animals in the fall and winter of 1918 and the spring and summer of 1919. While contemporaneous with the epidemic of influenza, there was no reason whatever to surmise a common etiology. It had occurred many times before in the laboratory. The duration of the disease was variable; most animals succumbed at the end of from 5 to 7 days. Early there was loss of appetite and a thin, watery nasal discharge, accompanied by frequent sneezing. The discharge descended from the nares to the breast and anterior extremities and, as the disease progressed, became mucoid and purulent in character. Animals used for experimental purposes (infections, vaccine injections, etc.) appeared more susceptible and succumbed 6 to 48 hours earlier as a rule.

STUDIES ON EXPERIMENTAL PNEUMONIA

STUDIES ON EXPERIMENTAL PNEUMONIA

THE PATHOLOGY OF EPIDEMIC PNEUMONIA IN MICE AND GUINEA-PIGS

The subject of epidemic pneumonia has been receiving a great amount of attention since the recent epidemics of streptococcus pneumonia and influenzal pneumonia. There are still many unknown factors of pathogenicity, virulence, invasiveness and toxicity of microorganisms which produce epidemic diseases. These terms commonly are used without clear distinction of meaning.1The difficulty of reproducing characteristic epidemic lesions or even causing infection in animals with cultures of highly specialized strains of bacteria is well known. In view of these difficulties in experimental reproduction of an epidemic disease, it has seemed possibly more profitable to study the natural processes of an animal epidemic of pneumonia, followed through its entire course of development and subsidence. The opportunity to observe and study such an epidemic presented itself in the animal room of the U. S. Naval Hospital, Chelsea, Mass., during the late winter and early spring of 1919. Distemper and epidemic pneumonia in

BLOOD CHEMISTRY STUDIES IN INFLUENZAL PNEUMONIA

Heretofore studies in blood chemistry have chiefly been confined to cases presenting evidences of renal involvement. Cases of pneumonia and other infectious diseases have received little attention in this direction. This is due to the assumption that such studies would be of little value, and partly also to the relative newness of the subject of blood chemistry. This report sets forth the findings in 131 specimens of blood from sixty-one cases of influenzal pneumonia, representing various degrees of severity, and obtained on various days of the disease. The results were obtained from forty-two nonfatal cases and sixteen fatal cases, thirteen patients receiving intravenous injections of hypertonic glucose solution and six cases receiving intravenous injections of foreign protein. Nonfatal Cases: Table 1 includes the blood chemistry findings in forty-two nonfatal cases, arranged according to the day of the disease on which the blood was examined. In a few of these cases

EFFECT OF INTRABRONCHIAL INSUFFLATION OF ACID

Acid administered to rabbits by intrabronchial insufflation causes an immediate and extreme damage of the lung tissue. Within certain limits the degree and extent of the injury vary according to the concentration of the acid. With the greater concentrations death occurs promptly, almost immediately, and the lethal process has associated with it a decreased permeability of the pulmonary vessels. The latter fact has been confirmed by postmortem arterial injections. With weaker solutions the results, grossly and histologically, resemble those noted after influenzal pneumonia and gas poisoning. Thus, there is destruction of the epithelium of the bronchioles, the alveolar ducts, and the alveoli. The extent of the damage to the alveolar walls varies. Exudation occurs into the alveolar, interstitial, perivascular, and peribronchial tissues. Primarily this exudate is serous, but a rapid deposition of fibrin occurs, and later polymorphonuclear leucocytes and erythrocytes accumulate. In different animals, or in different portions of the same lung, there may be consolidations of different types, serofibrinous, hemorrhagic, or purulent, with or without destruction of the alveolar walls. Subsequent changes relate to the organization of the exudate, necrosis, proliferation of the epithelium in the alveoli and bronchi, and, finally, to the regeneration of the pulmonary parenchyma. Experiments now in progress indicate that similar changes can be induced by various acids, both inorganic and organic. Experiments also show that similar changes are produced in other species of animals but that species differ in their resistance according to the acid and the concentration in which it is employed.

PRODUCTION OF PULMONARY INFARCTS BY THE INSUFFLATION OF ACID

Intrabronchial insufflation of acid causes immediate necrosis of the walls of many alveoli. Thrombosis of the alveolar vessels is an associated phenomenon. When a large number of vessels becomes affected, a clot propagates rapidly into the larger supplying vessels. The resulting lesion is indistinguishable from a hemorrhagic infarct. The infarct-like areas so frequently encountered in influenzal pneumonia, it is not unlikely, have their origin in a similar process. Infarction depends not only upon thrombosis or embolism of the large vessels, but may be initiated by extensive damage to the capillary bed. By this process infarcts may form in organs which are normally protected by collateral circulation.

Studies In Influenza and pneumonia: VI. The leukocytic reaction in influenza and influenzal pneumonia

Journal Article Studies In Influenza and pneumonia: VI. The leukocytic reaction in influenza and influenzal pneumonia Get access E. C. Rosenow E. C. Rosenow Division of Experimental Bacteriology, The Mayo Foundosion, Rochester, Minnesota Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 26, Issue 6, June 1920, Pages 492–503, https://doi.org/10.1093/infdis/26.6.492 Published: 01 June 1920 Article history Received: 28 February 1920 Published: 01 June 1920

Studies in influenza and pneumonia: Study v. Observations on the bacteriology and certain clinical features of influenza and influenzal pneumonia

Studies in influenza and pneumonia: Study v. Observations on the bacteriology and certain clinical features of influenza and influenzal pneumonia

INTRAVENOUS INJECTIONS OF HYPERTONIC GLUCOSE SOLUTION IN INFLUENZAL PNEUMONIA

One of the trying experiences of the medical profession during the late pandemic of influenza was the apparent helplessness in the treatment of the chief complication, pneumonia. The experience at the Camp Travis Base Hospital probably paralleled that of other similar institutions. At first, only the commonly accepted methods of treatment were used; but it soon became evident that some additional measures must be employed, else a very high mortality would result. At this hospital, resort was made to the use of quinin because of its recognized pneumococcidal action, and to the intravenous injections of hypertonic glucose solution. The results following the quinin medication are to be reported by others. The good results following the glucose treatment are attested by a relatively low mortality. This report deals with the results obtained in 319 cases of influenzal pneumonia, in which one or more injections of a sterile hypertonic glucose solution were

THE PATHOLOGICAL CHANGES IN THE TESTES IN EPIDEMIC PNEUMONIA

The testicular changes in pneumonia are without clinical manifestations, are non-specific, focal in character, independent of the infecting organisms or the antecedent disease, and vary in severity directly with the total length of the illness. The process is a continuous one, divisible into stages in which the following features are recognizable: (1) cessation of spermatogenesis; (2) degeneration of preformed spermatocytes, spermatids, and spermatozoa; (3) desquamation of altered cells and fragments of the same; (4) formation of giant cells in the tubule walls with subsequent liberation into the lumen; (5) disappearance of all desquamated cells and all those derived from the spermatogonia by mitosis; (6) in some instances thickening of the hyaline layer of the basement membrane. Older lesions are frequently found which continue the structural alteration of the tubules by hyalinosis and destruction of cells until they ultimately disappear. These lesions are not believed to be connected with the present illness. Edema may represent the acute injury in another form, and round cell infiltration suggests that possibly other factors than toxins may have a part in the tissue alterations. In the absence of definite evidence to the contrary, the cause is assumed to be circulating toxins, as Wolbach (12) claims for influenzal cases. The hemolytic streptococcus produced more extensive changes, both epithelial and interstitial, in primary pneumonia occurring during the measles epidemic than when pneumonia followed as a secondary infection; in the latter cases the pulmonary complications covered a relatively shorter period. Measles and epidemic influenza had little apparent effect upon the testes, except that the former caused mild inhibition of spermatogenesis; evidence regarding the latter is inconclusive. The Pfeiffer bacillus was always associated with other organisms, in primary infections and in those following measles. It occurred alone in a few cases after epidemic influenza, but the testicular lesion was not distinctive. The pneumococcus when alone in primary infections or after an epidemic disease produced a uniformly mild picture which was not intensified when associated with the influenza bacillus. Giant cells were much more frequent after influenzal pneumonia regardless of its cause and were associated with large numbers of other desquamated cells. They are formed in the walls of tubules by futile mitotic effort and incomplete protoplasmic separation, the abnormality of the process being further suggested by the early severing of cytoplasmic attachments and rapid desquamation. The series is unique in its uniformity, in the care exercised in the bacteriological examinations, and in the relative freedom from complicating factors.

VALUE OF CONVALESCENT BLOOD AND SERUM IN TREATMENT OF INFLUENZAL PNEUMONIA

The futility of usual forms of treatment during epidemic of influenzal pneumonia was early manifest. With a fatality much greater than our common pneumonia, it suggested pandemics of old when the pestilence stalked at noon day through city, and doomed inhabitants fell like grass beneath its scythe. Though causal agent was undetermined, it seemed that serum of convalescents might possibly contain antibodies in sufficient quantities to influence favorably course of disease. Serum from patients convalescent from scarlet fever was found by Huber and Blumenthal, Von Leyden 1 and others to be of some therapeutic value in that disease, and both experimentally and in human beings serum of poliomyelitis convalescents is beneficial if used early. 2 Richardson and Connor 3 recently demonstrated that serum of patients convalescent from measles conferred a certain amount of immunity. We did not know at

STATUS OF PROPHYLACTIC VACCINATION AGAINST INFLUENZA

When we consider the tragic experience through which the country and, indeed, the world, has passed during the last year, we realize that a great advance in preventive medicine would be made by the discovery of a prophylactic agent which would enable health authorities to control effectively epidemic influenza or the pneumonia that so often occurs as a complication. Perhaps at the outset it may be profitable to take stock of what we know about the etiology of influenza and the etiology and pathology of influenzal pneumonias. OPINIONS AS TO ETIOLOGY OF INFLUENZA AND INFLUENZAL PNEUMONIA Though the organism described by Pfeiffer in 1891 has long been known as the influenza bacillus, there really never has been convincing evidence of its relation to influenza, and the data that accumulated during the epidemic or epidemics here and abroad this past year have not contributed any confirmation to the view that this

ON THE CLINICAL EVIDENCE OF INVOLVEMENT OF THE SUPRARENAL GLANDS IN INFLUENZA AND INFLUENZAL PNEUMONIA

During the recent epidemic of influenza and influenzal pneumonia, we were impressed with the marked degree of asthenia present in all cases. No matter how mild the attack, asthenia was almost invariably one of the most, if not the most, prominent symptom. It was usually out of all proportion to the other symptoms and persisted not only during the attack but far into convalescence. When we review the summaries of chief complaints recorded in the literature, we find that this was the general observation. Certain symptoms were more common in some localities than in others, but asthenia was the symptom common to the disease in all localities. In our series of cases 1 we were unable to satisfy ourselves with the prevailing belief that the prostration was due to cardiovascular disease. Our attention was called to the possible existence of disturbed function of the suprarenal glands early in the epidemic, whereupon

INTRAVENOUS INJECTIONS OF FOREIGN PROTEIN IN INFLUENZAL PNEUMONIA

This report deals with the results from the intravenous injection of a foreign protein in eleven cases of influenzal pneumonia. Nine of the patients were critically ill and presented a grave prognosis. The protein used consisted of typhoid bacilli, macerated and exposed to the soluble action of alcohol for twelve hours, washed free of alcohol and suspended in physiologic sodium chlorid solution, the concentration being the equivalent of approximately three million bacilli per cubic centimeter. The dose employed was sufficient to produce a definite, so-called protein reaction, as a rule 1 c.c. Leukocyte counts were made previous to the injections, and from four to twelve hours following the reaction. In several cases blood chemistry determinations were made before and after the injections. From thirty to forty-five minutes after the injections the patients experienced a typical protein reaction, characterized by a severe chill and moderate cyanosis, lasting from fifteen to twenty

DISSEMINATED NECROSIS OF THE PULMONARY CAPILLARIES IN INFLUENZAL PNEUMONIA

One of the difficulties in attempting to find an explanation of either the hemorrhage or the huge edema¹of the lungs in influenzal pneumonia is that many different stages are encountered, most of them well along or late in the disease. Very early in this attempt, attention was directed to the presence of a layer of fibrin close to the lining of the alveoli and ducti alveolares, often a very thin layer and in some instances the only fibrin present. With lobar pneumonia (by this term I mean a disease which is lobar pneumonia not only anatomically but also clinically), such a limitation of the fibrin deposit to the alveolar lining is not common. Another outstanding condition is the necrosis of the alveolar lining epithelium, which appears early as a hyaline layer in which the outline of the separate cells is entirely lost, thus becoming a layer of necrotic