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History of Influenza Ch 3 Unique Clinical Symptoms

mixin

Well-known member
This chapter is a 40+ page look at how truly complicated this flu was. The author goes into great detail regarding the clinical features. I would really be interested in a modern-day doctor's opinion of this chapter.
http://influenza.sph.unimelb.edu.au/MOH_TOC.php

Jonsie's link here http://www.flutrackers.com/forum/showthread.php?t=23250 lists the usual symptoms that were seen here in the U.S. and I thought it was interesting to compare those to what this English doctor saw. Following are a number of his observations; (some are his words, some are mine).

His opinion of the numbers of those infected followed those of the U.S.:
Of 1,000 individuals striken by the disease, 800 had no more than an ordinary attack of uncomplicated "influenza,". It was the remaining 200 who were so much more seriously ill, with " pneumonic" symptoms added to those of simple influenza ; and of these about 80 died. The most dreaded symptom was the heliotrope cyanosis ; it developed in less than half of the pulmonary cases,but once it became definite the prognosis was so bad that I should say out of every 100 " blue " cases 95 died.

The inconstancies of the pandemic influenza are written about often:

# The rate of breathing became accelerated out of all proportion to the physical signs; in the worst cases the respiration rate would rise to 40, 50, or even 60 to the minute, and yet without any particular evidence of respiratory distress; orthopnea was exceptional and although the patients were breathing so rapidly they seldom, if ever, complained of actual difficulty in breathing; it was rather a frequent breathing?a polypnoea or tachypnoea?than a true dyspnoea.

# Speaking of when the pneumonic complications occurred in the course of the attack, he says all types were seen in abundance?the initial, the early, the later, and the latest.

# The condition of the skin could be either hot and dry or profusely sweating

# The pulse rate, though raised, was seldom unduly rapid, and it was a remarkable feature of a great majority of the cases that the condition of the pulse remained good almost to the last, falling only in articulo mortis.

# The only pattern the cyanosis followed was almost anyone who had it died; aside from that, in some cases it came on in less than 24 hours and the patient died within that time, sometimes, it was 48 hours, other times, patients lasted as long as a week.

# On studying many hundreds of consecutive charts (body temperature)there was nothing in the temperature chart itself to tell one whether the patient was doing well or badly.

# The sputum was very variable indeed. The same patient might bring up different types of sputum on successive days, and in the same ward successive patients, suffering apparently in a similar way, might be bringing up each a different type of sputum, so that no conclusion could be drawn from the appearances of the latter as to what degree of the malady the patient had.

# As a general rule what struck one most was the frequent paucity of abnormal signs, when the degree of illness of the patient led one to expect many.

# Delirium and coma occurred often enough amongst the bad cases, but far more striking than their occurrence was their entire absence almost to the very end in so many instances. When delirium did occur it was seldom of the noisy, trembling, shouting-out type, though cases of this sort occurred too. More often it was of the low muttering restless type, the patient picking at the bed clothes and at objects round about him, with rambling talk or incoherence ; getting out of bed, but readily getting back when asked to ; rational for a few moments when spoken to, able to answer questions, and yet lapsing quickly into a restless semi-conscious state when left. Anothertype of case became totally unconscious hours or even days before the end, restless in his coma, with head thrown back, mouth half open, a ghastly sallow pallor of the cyanosed face, purple lips and ears?a dreadful sight.

# Subsultus tendinum was a marked phenomenon in many cases quite apart from delirium or coma. The patient might be rational enough to be talking about himself and he might even himself call attention to the way he could not keep his legs or arms or back muscles quiet when he wanted to. A leg or an arm or the abdominal muscles or the back would give an involuntary twitch or jerk; or the face or one shoulder, or some other part; the character of the condition approaching in a few instances almost to that of mild chorea. As a rule the prognosis proved bad, though the patient was by no means always in extremis when the symptom first developed.

# The kidneys in almost all the fatal cases showed acute nonsuppurativenephritis, milder in degree perhaps than that met with in scarlatina, but similar in type. Few cases, however, presented the ordinary clinical picture of acute nephritis for there was no oedema to attract notice. It is probably too much to say that no case of generalised nephritic oedema occurred at all; but I saw none, even when acute nephritis was demonstrated post-mortem.

(I thought his comments on pus formation was especially interesting so I've included his entire comment.)

# Localised Pus Formation. Acute pleuritic effusions, generally small in amount and yielding turbid fluid rather than definite pus, were quite common in the " pneumonic " cases ; this turbid fluid contained X3olymorphonuclear cells microscopically and yielded cultures of pneumococci, diplo-streptococci, or streptococci bacteriologically, but it was not very common for these effusions to develop into definite empyemata. Many such effusions, though containing turbid fluid, excess of leucocytes and micro-organisms resolved spontaneously ; some were found post-mortem in the fatal cases, but a few became definite empyemata, and it was noted as a rather remarkable feature of such cases that once definite pus developed in the chest, the patient ultimately did well, no matter how ill he might appear to be at the time.

The same seemed true of other cases in which localised collectionsof pus developed elsewhere than in the chest. In two or three instances, for example, successive subcutaneous abscesses, py?mic in type, had to be opened and drained with recurrence of fresh abscesses for several weeks, and yet, after a time of great anxiety, the patients made a complete recovery.

In another type of case?quite exceptional?subcutaneous suppuration developed at the site of saline injection. Almost without exception any patient in whom any local abscess or empyema or similar focal suppuration occurred, ultimately did well. To such extent did this impress more than one observer that deliberate attempts to produce a spontaneous abscess, not by injecting extraneous organisms but by focalising the patients' own organisms, were made in the belief that if such " fixation " abscesses could be produced, the patients would do as well as those in whom spontaneous suppuration occurred. When, however, one tried to produce suppuration in this way by trauma, or by the subcutaneous injection of irritants such as turpentine, one did not once succeed in obtaining a local " fixation " abscess ; and yet it is a point that merits special emphasis, that whenever spontaneous suppuration did develop in these influenzal " pneumonic " patients, one could almost invariably assume that the patient was going to pull through and get well, even though his actual state at the time might otherwise look precarious.

# Regarding oxygen masks he says: One wonders whether in future cases, should they occur, it would not be a better plan to give the oxygen through soft rubber catheters inserted through the nostril so that a constant stream of oxygen might thereby pass into the patient's respiratory passages without producing that sense of oppression and suffocation that the patients complain of when wearing a face mask. I saw no cases treated in this way, but I think it would be a procedure worth a trial should any similar occasion arise, using the technique described by Stokes and Ryle (Guy's Hospital Gazette, 9th August 1919) in connection with cases of acute gas poisoning in France. (I wonder if this could be done in a pandemic with vent shortages?)

Here might be a case for the benefits of vitamin D:
# In some hospitals where there was immense strain upon the available beds, it became necessary to put the worst, and apparently hopeless cases, elsewhere, and one saw scores of extremely bad cases transferred from the wards to the quadrangles out of doors, under waterproof canopies, and whereas at first one felt that this? though a necessary procedure?would at least not help any of these dire cases to get better, one found to one's surprise that a larger number of those very worst cases put out of doors did, as a matter of fact, recover than would have been the case, one felt sure, had they remained indoors.

I thought his remarks here summed up the frustration the doctors of that time must have felt:
# "One feels tempted to coin a new word altogether to express so complete a type of lung-inflammation, and to term it "pneumonitis" ; for no part of the lung tissue seemed to escape. One could then speak of the lesions as
being of such varying types as the following :?
"Pneumonitis," with preponderance of congestion and oedema, but with little or no consolidation ;
"Pneumonitis," with much congestion, bronchitis and some broncho-pneumonia in the lower lobes ;
"Pneumonitis," with preponderance of congestion, interstitial haemorrhage, oedema, and collapse, but little broncho-pneumonia ;
"Pneumonitis," with congestion, haemorrhages, collapse, and extensive broncho-pneumonia;
and so on.
 
Re: History of Influenza Ch 3 Unique Clinical Symptoms

it was noted as a rather remarkable feature of such cases that once definite pus developed in the chest, the patient ultimately did well, no matter how ill he might appear to be at the time.

thank you.. I m very surprise about it and I had the notion that fixation abscess had good results ( bad notion )
note : diplo streptococcus : is pneumococus, it is the same or Streptococcus Pneumoniae : gram positif.

thank you for post-mortem description ( anatomopathology? ) which is a little disturbing.

there seems to be at least 2 entities, at several stages of evolution ?
 
Re: History of Influenza Ch 3 Unique Clinical Symptoms

Some of his descriptions are pretty graphic; he goes into great description about lung tissue and sputum also.:D He says: "I also performed, or was present at, autopsies totalling over three figures."

Having no medical background, I didn't understand exactly how all the symptoms related to influenza and the secondary infections.
 
Re: History of Influenza Ch 3 Unique Clinical Symptoms

he goes into great description about lung tissue and sputum also.

at which page ?

yellow sputum ( or green ) with or without blood : bacterial infection.
can be more or less thick, and adhere to the spittoon ( it is better sign when it is fluid )
at the beginning of peumonia the patient does not spit, no sputum
sorry for description at morning..:D

for example : consolidation indicates that the lung has the consistency of the liver, because it is filled with pus, blood, bacteria etc..
At percussion, it resonates as liver.
 
Re: History of Influenza Ch 3 Unique Clinical Symptoms

3 large pictures of heliotrope cyanosis on page 10
sputum on page 14
Lungs on page 17, mostly on page 37-41
 
Re: History of Influenza Ch 3 Unique Clinical Symptoms

all chapter 3 is very interesting.
this doctor write very well, as all doctors at this time , and saws thousand cases.
the most were mild cases as he said, it was " normal influenza" .

it gives the overall impression that "pneumonia" was bacterial , but different from classical pneumococcal pneumonia or from pneumonia from 1915 or 1916 because of severity.
No real treatment, nursing.

No description of cytokine storm ( or something equivalent )
septicemia
the autopsy showed lesions that this doctor had never seen before ...patched, mixed, at different stage of evolution ( no real consolidation )

the taxinomy of bacteria ( or denomination ) was different in 1918..

about bacteria and pneumonia in 1918.
modern article

http://www.journals.uchicago.edu/doi/full/10.1086/591708#tb1
snip

Surprising aspects of 1918–1919 influenza-associated pneumonia fatalities included the following: (1) the high incidence of secondary pneumonia associated with standard bacterial pneumopathogens; (2) the frequency of pneumonia caused by both mixed pneumopathogens (particularly pneumococci and streptococci) and by other mixed upper respiratory–tract bacteria; (3) the aggressiveness of bacterial invasion of the lung, often resulting in “phenomenal” [30] numbers of bacteria and polymorphonuclear neutrophils, as well as extensive necrosis, vasculitis, and hemorrhage [20, 32, 33]; and (4) the predominance of bronchopneumonia and lobular pneumonia, as opposed to lobar pneumonia, consistent with diffuse predisposing bronchiolar damage [2733].

snip


. As was true for the 58 autopsy cases we reviewed (see above), published autopsies for victims of the 1918–1919 pandemic generally showed histopathological asynchrony [20]. Repair, represented by early epithelial regeneration, capillary repair, and occasionally by fibrosis, was commonly seen in tissues sections from even the most fulminant fatal cases [20, 27, 32]. Among the
2A7E.gif
60% of individuals who survived such severe pneumonia, severe chronic pulmonary damage was apparently uncommon [37, 38].

snip

In the 14 of 96 autopsy series that did not report the predominance of lung pneumopathogens [29, 36, 4153], pneumopathogens accounted collectively for 37.4% of pneumonia deaths. The rest of the deaths were associated collectively with either culture of nonpneumopathogenic “other bacteria,” such as nonhemolytic and viridans streptococci, “green-producing streptococci” [54], probably largely corresponding to α-hemolytic streptococci, uncharacterized diplostreptococci, Micrococcus (Moraxella) catarrhalis, Bacillus (Escherichia) coli, Klebsiella species, and complex mixed bacteria (36.1% of cultures). Cultures also yielded Bacillus influenzae (18.8%) and no bacterial growth (7.7%).

The predominant coinfecting microorganism in lung tissue cultures containing
2A7E.gif
1 pneumopathogen was Bacillus influenzae (largely corresponding to the modern Hemophilus influenzae), an upper respiratory–tract organism not commonly found in pure culture of samples from any anatomical compartment [20, 36, 55].
We believe that the weight of 90 years of evidence (table 3), including the exceptional but largely forgotten work of an earlier generation of pathologists, indicates that the vast majority of pulmonary deaths from pandemic influenza viruses have resulted from poorly understood interactions between the infecting virus and secondary infections due to bacteria that colonize the upper respiratory tract. The data are consistent with a natural history in which the virus, highly cytopathic to bronchial and bronchiolar epithelial cells, extends rapidly and diffusely down the respiratory tree, damages the epithelium sufficiently to break down the mucociliary barrier to bacterial spread, and if able to gain access to the distal respiratory tree—perhaps on the basis of receptor affinity [80]—creates both a direct pathway for secondary bacterial spread and an environment (cell necrosis and proteinaceous edema fluid) favorable to bacterial growth. It remains unresolved whether cocolonizing, nonpneumopathic upper respiratory–tract organisms such as Bacillus (Hemophilus) influenzae play an ancillary role, or are merely innocent bystanders. It is uncertain why Hemophilus influenzae was much less prominent in 1957–1958 and thereafter, but this phenomenon may relate to antibiotic use and conceivably, in recent years, to Hemophilus influenzae b vaccination of children.
The extraordinary severity of the 1918 pandemic remains unexplained. That the causes of death included so many different bacteria, alone or in complex combinations, argues against specific virulent bacterial clones. The pathologic and bacteriologic data appear consistent with copathogenic properties of the virus itself, perhaps related to viral growth, facility of cell-to-cell spread, cell tropism, or interference with or induction of immune responses. Certain observers believed that cotransmission of the influenza agent and of pneumopathogenic bacteria was responsible for many severe and fatal cases, especially during the October–November 1918 peak of mortality and case-fatality rates [81].
We speculate that any influenza virus with an enhanced capacity to spread to and damage bronchial and/or bronchiolar epithelial cells, even in the presence of an intact rapid reparative response, could precipitate the appearance of severe and potentially fatal bacterial pneumonia due to prevalent upper respiratory–tract bacteria.
 
Re: History of Influenza Ch 3 Unique Clinical Symptoms

Anne, from your post: It is uncertain why Hemophilus influenzae was much less prominent in 1957?1958 and thereafter, but this phenomenon may relate to antibiotic use and conceivably, in recent years, to Hemophilus influenzae b vaccination of children.

From what I've read, Hemophilus influenzae (Pfieffer's bacillus) was included in many of their vax formulations. I wonder if it was found frequently between 1919 and 1957?

The vaccines back then were interesting; were they live?
 
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