THE PATHOGNOMONIC COURSE AND SYMPTOMS
Lobar Pneumonia
Broncho-Pneumonia
Bronchiolitis
Varieties of Pneumonia


THE PATHOGNOMONIC COURSE AND SYMPTOMS

Since clinical differentiation became more exact at the turn of the 19th to the 20th century, due to the technical progress in medicine, e.g. X-ray images for pneumonia diagnostics, many descriptions in the medical literature of the 19th century seem more vague in their classification.
Other terms were also used to differentiate pneumonia, which seem obsolete today, but are crucial for understanding these historic descriptions.
The mentioned terms are explained in detail in the glossary and assigned to the corresponding time periods. glt1,2023

As always in homeopathic medicine, it is very important to obtain the individualizing features of the case in order to prescribe appropriately.
The individual symptoms, signs and process-features differentiate the case of the patient with pneumonia being treated here and now from a standard-case (pathognomonic symptoms and disease-course).
We attempted to put together the most profitable clinical observations to present the standard-course of the disease and thus helping you to identify the individualizing features for successful homeopathic treatment.


Lobar Pneumonia

Old synonyms: Croupous, Fibrinous pneumonia, Pneumonic fever

General Course

The following descriptions are taken from Paige's pew1,1904 book.
Otherwise it is explicitly noted.

Prodromal stage:
There is, as a rule, no pronounced period of invasion or prodromic symptoms.
The patient may have experienced slight feeling of malaise and depression with some mild symptoms of a catarrhal nature.

First stage/congestion (1 st day):
But in lobar pneumonia, more marked than in any other disease, the invasion is sharp, decided and severe.
The patient is seized without warning while at work, during sleep or other unexpected time, with a pronounced and severe chill [Look out for chill-symptoms/rubrics like "Chill beginning in hands", etc.! glt2,2023].
Even during the chill the thermometer shows the fever is rising.
Shortly after the onset the patient shows flushed features, headache [- headache, with nausea, vomiting, and with delirium and convulsions in children bwax,1902], and general pains.
[Almost without exception with the onset of chill, the muscle forces have diminished, making it almost impossible for the sick person to maintain himself. bhb2]
Within a few hours a sharp chest pain develops of an agonizing character due to the associated pleurisy.
A short, dry, painful, hacking cough begins with scanty rust colored expectoration [, clear or missing sputum or bloody from the beginning - from tingent blood to just blood to rusty old blood snex].
The temperature rises to 104° - 105°F/40-40,6°C [usually continual fever over a week glt1,Herold,2017].
Vertigo and congestional symptoms can be present.
[In children - Fever can rise again after it has fallen by 1-2°C/1,8-3,6°F. Lung-restriction in affected side, breathing-effort also in cervical muscles, tension in Musc. trapezius.
On auscultation we find broncho-vesicular breathing in the beginning then crepitation.
Percussion-sounds are unremarkable in the beginning, then there is a higher sound and finally dullness. gccx,1902]

Second stage/hepatization (2 nd - 5-7 th day - 2 nd - 3 rd day red hepatisation (infiltration rich in red blood cells), 3rd till 7th day yellow/grey hepatisation (infiltrate rich in white blood cells):
By the second or third day the patient presents a very characteristic appearance.
He lies flat in bed, usually on the affected side, as the pressure eases the pain and gives the well side more play in respiration.
The breathing is hurried and labored [the breathing difficulties with weakness are dominant in this stage glt2], the alae nasi distended with each inspiration and a short expiratory grunt accompanies each expiration.
The cough is frequent, dry, racking and causing sharp pain, so that he winces and holds his side with the characteristic rusty and very tenacious expectoration [; sputum more and yellow, dark yellow and then green, all kinds of tastes to this sputum snex].
The face is deeply flushed, especially upon the cheeks, with herpes about the lips.
The skin is hot and dry, the eyes bright and shining, and the expression very anxious.
The temperature is usually 104° to 106°, the pulse full and bounding, and its ratio out of proportion to the rapid respiration.
[In severe cases there might be delirum.
Hydration and renal function might be difficult at this point. glt2] There are all the signs of consolidation in the lungs, bronchial breathing and crepitant rales.
[Feeling of constriction in the chest.] dicx Sleep is often just a exhausted doze not a sound sleep.
[There is increasing breathing-excursion on the not affected side.
Vocal fremitus is palpable over affected areas.
On percussion we find marked attenuation, change of sound with open or shut mouth.
Dull resonance with pleural effusion at the base of the lung with ascending dullness of percutory sounds.
On auscultation we have a lot of moist rales in all varieties, also crepitation is loudly audible; bronchophony on "99". gccx,1902]

Third stage/resolution (5-7 th till 10-11 th day):
Massive exhaustion with stress on the cardiac system.
It terminates by crisis or lysis - crisis is often the first day of lysis, because the fever can lead to cardiac failure at that point, which is the most common cause of death in this disease.
[Lysis means encymatic liquification of the infiltrate with coughing up sputum.
There can be accumulation of sputum with specific modalities due to large quantities of sputum.
This can lead to a state where the metabolism is flooded with waste products of the infection and often leads to deep exhaustion glt2], the temperature falls with a rapid return to a sense of comfort.
Sweat can be prostrating.
Sleep is still disturbed.
[In the third stage the sputum goes the other way, so reverse order: from green to yellow, to light yellow, to clear and less. snex] [Vocal fremitus decreases, re-establishing breathing mobility; On auscultation: Decreasing crepitant sounds for 3 week.
We find gurgling sounds if there is formation of lungs abscess.
On percussion different Dullness can be percieved in various regions for a long time during reconvalescence.
On auscultation we hear successively re-ventilation with broncho vesicular breathing sounds.
A recurrent rise of temperature after the 8th day is often a sign of formation of lung-abscess. gccx]

Fourth stage/reconvalescence:
Regeneration of the lungs, stabilization of the cardiac system and re-establishment of sound sleep (means for example that dreams are again remembered in the morning).
Full resorption of fibrinous exsudation takes 4 weeks.
If this reabsorbation is missing out this can lead to irreversible induration of the lung tissue.

Take care: If the patient was treated with antibiotics, the morphological lung-changes are not shortened in time.
Therefore caution the patient to avoid physical exertion too early, since otherwise relapse or other complications may arise! If the condition of the patient is not ameliorated within 48h after begin of antibiotic treatment, it is clear that this antibiotic is not curative and the inflammatory process in the lungs is still advancing.
Still even when the antibiotic is helpful it takes 3-5 weeks bbefore the patient is cured.
This can be seen through the persisting general symptoms like weakness and sweating. glt1,Herold,2017

Now to examine the symptoms in detail:

The Fever:
Rises rapidly after the chill and may reach its acme in twelve hours, but is usually at its height by the second day.
Having reached 104° - 105°F/40-40,6°C it remains very constant with morning remissions from 1 to 2°F or 0,6-1,2°C.
In the aged and inebriates the temperature runs lower than in children or the robust.
There are rare cases with a very low degree of fever.
During the chill, especially in old people, the shock may be so severe that unconsciousness or collapse symptoms may appear.
The day of the crisis is variable.
In some cases it may occur as early as the third day, while in others it may be delayed until the twenty-first day.
These tedious cases, however, are usually caused by an extension of the inflammation to new areas or complications in other organs.
The usual time for the crisis is the seventh or eighth day and it should be expected at that time.
The very rapid fall of temperature in pneumonia is striking.
In most cases it only takes about twelve hours.
The fever will fall from 104° - 105°F/40-40,6°C to normal or below, accompanied by a profuse perspiration; the pain, cough, respiratory distress all disappear promptly and the patient falls into a quiet, natural sleep.
The peculiarity of it is that all this occurs without any perceptible change in the condition in the lung itself.
In some instances the temperature falls so rapidly, occupying only five or six hours, to normal or even lower (to 96°F/35,6°C or 95°F/35°C), accompanied by vomiting, diarrhoea, profuse cold sweat, [,copious discharge of urine takes place bwax,1902], that a condition of collapse maintains.
[Ed.: crisis] In other cases two or three days are required for the return to normal, this is particularly true since influenza made its appearance.
There may be a slight rise for two or three hours before the crisis, and again after the crisis there may be a slight rise to 101° or 102°F/38,3 or 38,9°C.
This is doubtless due to contamination of the blood by the absorption of the exudation.
A pronounced rise of temperature to 102° or 104°F/38,9-40°C after defervescence indicates that the disease has invaded a new lobe, or the occurrence of pleurisy, empyema, gangrene or abscess.
If the fever lasts until the twelfth day, the decline is by lysis; this is especially apt to occur in the case of children.
If resolution is protracted the temperature may maintain over a period of several weeks.
In debilitated persons a rapid fall sometimes precedes death and should not be mistaken for the crisis.
Usually, however, a rapid rise precedes dissolution.

Chestpain:
Is due to the attending pleuritis.
This is absent in central pneumonia, but marked in inflammations near the surface.
It is very sharp and distressing usually just below nipple of the affected side - also found in axilla and posteriorly under the scapula.
[It may be in the lumbar and iliac region.] bwax,1902
With diaphragmal involvement the pain can extend to the right hypochondrium, in children also to the lower abdomen.
Here it has to be differentiated from appendicitis or acute abdomen!

Respiration:
Difficult and rapid, out of ratio to the pulse, usually runs from 30 to 40 per minute (in adults Ed.), while the pulse may be only 100 to 120 per minute.
May be as high 60 or 80 [; not increased in proportion to the respirations, and instead of the normal relation of 4 to 1 it may be 2 to 1. bwax,1902]
Inspiration is short and expiration accompanied by a grunt, while the chest movements on the affected side are limited voluntarily to avoid pain.

Pulse:
Heart failure is a possible complication in patients with pneumonia.
In patients with a healthy heart and uncomplicated course of the disease this is not often the case.
Risk factors are accompanying myocarditis or septic cardiomypathia, previous existing heart-diseases or a very severe course (very extensive infiltrate) of the pneumonia.
It may develop rapidly or slowly, and appear as early as the third day or during the crisis or thereafter.
Due to the effort of the heart to supply the system with oxygen, impeded by the occluded lung, high fever, and also to specific poisoning of the cardiac muscle by the bacteria.
In most favorable cases the pulse is 100 to 110.
Rates of 120 to 130 is a cause for apprehension.

Cough:
Is hard, frequent and restrained, accompanied by great pain and after first few hours with a characteristic viscid, blood tinged and very tenacious expectoration.
[In the first few days it consists of a frothy mucus; by the third day it becomes thick, tenacious and of a rusty color]; bwax,1902 [This at first is viscid, transparent, and scanty, hut soon assumes a character distinctive of the disease.
It becomes adhesive and has a reddish tint like brick-dust or rust.
The adhesiveness is such that it cannot be poured from a vessel but remains attached to the bottom even when the vessel is inverted and shaken.] dicx In low types [esp. in aged and alcoholics bwax,1902] of the disease the expectoration may be dark fluid, resembling prune juice.
In some forms, especially in drunkards or the aged, the cough and expectoration may be absent.

Gastrointestinal symptoms:
Vomiting is quite common early in the disease, especially in children [- and during chill, in connection with tormenting cough or because of brain irritation (esp. during pneumonia with whooping cough) gccx,1902] Tongue is usually white and furred, but in some cases or late in the diseases may be dry and brown [and even to a black in those cases where the nervous symptoms predominate.] bwax,1902 Constipation is the rule with anorexia.
The spleen and liver may be enlarged, the latter, from the engorged right heart.

Urine:
Presents early the usual febrile symptoms of high color, increased specific gravity and acidity, with traces of albumin [and contains an excess of urea and uric acid; also blood and fibrinous casts] bwax,1902 .
A great amount of albumin is an unfavorable sign. glt1,2023 One characteristic and important diagnostic sign of pneumonia (unlike pleurisy with effusion or empyema) can be the diminuition or absence of chlorides in the urine.
This is connected with (de-)hydration of the body of the patient and other parameters.
[Quantity: The urine is diminished in quantity; there may be 1000 - 800 cc/ml.; sometimes even 400 cc/ml.
With the crisis there is increase, but restoration to the normal quantity is generally delayed several days.
In so-called "bilious pneumonia" bile is often present in the urine.] gccx,1902

Skin:
Herpetic eruption is very usual, especially about the lips.
[Ed. Nowadays - at least in central Europe this is a seldom concomittant - which can be seen as a homeopathically characteristic sign.] Profuse sweating at and immediately following the crisis is the rule.
The cheeks, particularly during the height of the disease, are markedly flushed, especially the cheek on the affected side.

Cerebral Symptoms:
Convulsions frequently usher in the disease in children.
Headache is very common.
As a rule delirium is not usual in pneumonia, but may develop in a low or severe type of the disease, especially in those with unsound kidneys and drunkards.
In some cases it becomes maniacal and in others, particularly in children, so resembles the symptoms of meningitis that the latter is diagnosed and the pneumonia overlooked.
Mental aberration may continue into and after convalescence.

Specifics in children mur1,2016,glt1,2

Viruses are important causes of pneumonia in both adults and children and can lead to bacterial superinfection or mixed infections.
They are estimated to cause 16% of total pneumonias in pediatric outpatients and up to 49% in hospitalized infants.
These figures may underestimate the importance of viral infections as a cause of pneumonia, particularly in outpatients, because of the insensitivity of viral diagnostic methods and because of the lack of chest radiographs in many patients with viral infections.
RSV, Parainfluenzavirus and Adenovirus, in addition to influenza viruses are the most important viral causes of pneumonia.
Measles virus pneumonia affects children and adults during epidemics in susceptible populations. mur1,2016

Galic glt2,2023: Bacterial cases more often lead to severe course, viral ones tend to have a prolonged course.

[Some cases of viral pneumonia have a rapid and relentless fatal course with generalized alveolar and interstitial opacities, development of Respiratory Distress Syndrome and progressive respiratory failure. mur1,2016]
In pre-term born children needing artificial respiration or children with chronic diseases of the lungs or heart like mucoviscidosis often opportunistic infectious agents are present.
[Adenoviruses cause a particularly aggressive form of pneumonia in neonates, characterized by necrotizing bronchiolitis and alveolitis.
The virus may be acquired from the mother, perhaps via the birth canal.
Long-term sequelae of adenovirus infection may include persistent radiographic abnormalities, abnormal pulmonary function tests, bronchiectasis, and bronchiolitis obliterans. mur1,2016]

Pneumonia in childhood is accompanied by more symptoms of the nervous system in severe cases.
Headache, delirium, or stupor are more often present than with diseased adults.
Convulsions often occur, especially at the onset of the disease, but may also appear later during its course, followed by delirium or semi-consciousness, with involuntary urination and defecation.
This may lead to errors in the diagnosis.
The presence of cough with short, labored, grunting respiration, which is very rapid (50 to 80 per minute), indicates a careful examination of the chest, lest a case of pneumonia be mistaken for one of the various forms of meningitis.

In nurslings you often see a suffering expression, apathy, nursing difficulties, problems with regulation of body-temperature (hypo- or hyperthermia).
Pneumonia is here often part of a septic state.

Infants often show tormenting cough with high fever, tachycardia, weakness, and night-sweats.
Severe breathing difficulty is indicated by the following: frequent, superficial breathing, sighing respiration, motion of alae nasi with breathing; circumscribed redness of the face, paleness around the mouth, eventually cyanosis of the lips.
In severe cases there might be peripheral cyanosis and swelling of the liver.

Take care: In pneumonia with formation of abscesses due to Staphylococcus there also might be distension of the abdomen, hardly any peristalsis (sometimes leading to ileus) or atelectasis due to excessive sputum.

Also consider the possibility of aspiration pneumonia - in nurslings most often due to vomiting, in infants most often due to foreign bodies!

Gatchell gccx,1902: The upper lobes are more frequently involved than in adults.
The initial chill is missing out, instead it often begins with serious vomiting with diffuse abdominal pain or convulsive shivering.
There is great variation of body-temperature with peaks of heat, very frequent pulse and rapid onset of drowsiness.
During summertime diarrhea is frequent at the beginning.
The combination of: High fever with quick respiration and pulse is very often a sign of pneumonia! Prognosis for children is unfavorable if - disease happens before 3rd year of life, fever is constant above 40,6°C/105°F, two lobes are involved, late onset of vomiting and convulsions arise during the course.
Examination at the beginnning often shows scarce clinical findings, the local symptoms become clearer in the course of disease.

Specifics in elderly and people addicted to alcohol mur1,2016

In older patients, especially those with multiple comorbidities, pneumonia may present with general weakness, decreased appetite, altered mental status, incontinence, or decompensation due to underlying disease.
The presence of tachypnea may precede other signs of pneumonia by 1 to 2 days.
Tachycardia is another common initial sign but is less frequent and specific than tachypnea.
Fever is absent in 30% to 40% of older patients.
Owing to the lack of specific symptoms, the diagnosis of CAP is frequently delayed in older adults.
Older patients with pneumonia who present with altered mental status without fever can have a delay in receiving antibiotics by more than 4 hours after arrival; this delay increases mortality. mur1,2016

In debilitated older patients, vague clinical manifestations of pneumonia are common and the presence of fever with no apparent source, especially when accompanied by confusion or tachypnea, justifies obtaining a chest radiograph.

Clues to the etiologic diagnosis may lie outside the respiratory tract.
Bradycardia in relation to the amount of fever (pulse should increase by 10 beats/min/°C of temperature elevation) has been associated with pneumonia due to Legionella, C. psittaci, Mycoplasma, or F. tularensis. [Ed. Compare Pulse/non-corresponding with temperature.]
M. pneumoniae infection may present with extrapulmonary manifestations including arthralgia, cervical lymphadenopathy, bullous myringitis, diarrhea, myalgia, myocarditis, hepatitis, nausea, pericarditis, and vomiting.
Skin lesions of erythema multiforme or erythema nodosum suggest Mycoplasma infection (as well as tuberculosis and endemic fungal infection), whereas lesions of ecthyma gangrenosum are most often seen with P. aeruginosa infection.
Finally, the examiner must look for the presence of complications such as pleural effusion, pericarditis, endocarditis, arthritis, and central nervous system involvement, which may necessitate further diagnostic procedures and, potentially, a change in therapy.

[Acute pneumonia in the aged and those with great lowering of the nervous vitality is often mistaken for typhoid fever, as the cough, expectoration, pain, and in some cases the dyspnea, may all be absent.
In these cases the physical examination of the lungs must be relied upon.

In people addicted to alcohol the symptoms of pneumonia may simulate those of delirium tremens and in such cases a careful physical examination is also demanded.] bwax,1902

[The beginning of the disease is often not clearly marked, symptoms often vague, fever is low and delirium might be the strongest sign of the disease-picture.
Only the thermometer can show that there is an acute disease.
Often the local disease process is overseen, because the patient does not complain of pain, dyspnea is often moderate, and cough and expectoration are missing.] osl1,1909


Broncho-Pneumonia

Former synonyms: Catarrhal pneumonia, Lobular pneumonia, Disseminated pneumonia, Capillary bronchitis
General Course

Etiology bwax,1902
It occurs more frequently during the winter and spring months [a typical trigger is wet-cold weather glt2].
This is the form of pneumonia met with among infants, children that are exposed to cold unsanitary surroundings, and those suffering from chronic diseases.
It is a frequent complication of the acute infectious diseases, especially measles, whooping-cough, influenza, diphtheria, typhoid fever, and smallpox.
In these cases the alveolar structure is involved, either by continuity or aspiration of the bronchial secretions.
Inhalations or insufflations of particles of food or other foreign material become active causes in those suffering from a low form of fever; and in the cases of the new born as a result of vigorous inspiratory efforts made while the head is descending through the vagina.
Inhalations of steam and irritating vapors are active causes, especially if the vapors hold decomposing organic matter in suspension; cutting of the vagus nerves, or tumors of any kind, by producing paralysis of vocal cords, allows the irritating secretions, particels of food and micro-organisms to be conveyed to the lungs during inspiration.
[Diseased children also often have a family-history of an atopic disease (like hayfever, allergic rhino-conjunctivitis, eczema or asthma).
Herein lies an increased risk of obstructive breathing for the child. glt2,2023]

Symptoms pew1,1904
The earlier symptoms are essentially those of the accompanying bronchitis of the smaller bronchial tubes.
It is sometimes very difficult to determine just when lung tissue becomes involved.
But when in the course of a bronchitis, whether simple or associated with some other disease, there is a gradual rise of temperature to 103°F/39,4°C or 105°F/40,6°C (but not the chill and sharp rise of fever seen in lobar pneumonia), [...is of an irregular type, and terminates by lysis, after a duration of from two to four weeks; bwax,1902] In some cases, after pursuing a moderate course for a time, the temperature will suddenly mount several degrees.
This variability of the temperature, which denotes extension at intervals into new territiory, is an important sign of the fever of broncho-pneumonia, and is to be taken into consideration in diagnosis and prognosis.
The temperature often rises as high as 104°F/40°C and 105°F/40,6°C. .
An idiopathic case is usually ushered in by a slight chill or a succession of chilly sensations.
There may be repeated chills, marking an extension of the disease-process in new areas of the lungs.
This symptom is always significant. .

Skin: is usually moist [and clammy sime,1890], with a tendency to perspiration. gccx,1902 .

Respiration becomes difficult and increases in frequency to 50 or 80 per minute, with the complaint of soreness and pain; the pulse grows rapid (140 - 160), loses force and is compressible [; sometimes irregular gccx,1902].

The soft, loose cough of the preceding bronchitis becomes dry, tight [, hacking, tormenting, glt2] and hard with pain [behind sternum] and deep soreness; [in young children cough is maybe absent gccx,1902] expectoration is slight or absent - if present it is muco-purulent or blood streaked (not "rusty" as in lobar pneumonia), then the invasion of a broncho-pneumonia may be diagnosed.
Fatal cases are due to the respiratory condition and symptoms.
The respiration become frequent, labored, feeble and short, the extraordinary muscles of respiration with the alae nasi are brought into play, the heart systole grows weaker with feeble pulse, clammy extremities and cyanosis, death occurring from heart failure due to respiratory failure. [.with cyanosis that affects the lips and conjunctiva, while later the face becomes dusky and the finger tips blue. bwax,1902]

Face: The countenance has an expression of dejection, with some redness of the cheeks, but without the dark-red suffusion so often met with in pneumonia. sime,1890 [Paleness, dark around the eyes. glt2]

The tongue is but slightly furred. sime,1890

Urine is scanty, sometimes albuminous. gccx,1902

In favorable cases the temperature lowers, respiration becomes deeper and less frequent and labored, the cough loosens, expectoration becomes freer and the pulse grows stronger.
In the chronic form the pulse and respiration gradually increase in frequency, the temperature is never as high as in the acute, rarely going above 102°F/38,9°C.
There is dyspnoea, loss of appetite, strength and flesh and a general systemic failure [esp. in children also with pallor, discoloration around the eyes, reduced energy, emotional instability.
This state and its phenomena has a marked similarity with the description of tuberculosis in historical literature.
The general condition is often much worse than the examinational findings. glt2,2023].
Death in such cases occurs from general exhaustion and cardiac failure, not from respiratory failure as in the acute form.

Findings on examination pew1,1904

Percussion shows isolated points of consolidation, vocal fremitus being increased over these areas.

Auscultation shows fine [and large bwax,1902] mucous rales over the [several glt2] affected areas, heard during inspiration and expiration and of a metallic character, indicating pulmonary consolidation.

[The vocal resonance and fremitus are intensified, corresponding, as a rule, to the area of percussion dullness.] bwax,1902

[On X-Ray peri-bronchitic striation can be seen.

In diagnostic for infectious agents most of the times not the classic pneumococcus is found, but instead less aggressive agents, like Mycoplasma.
Nevertheless these agents respond much less to antibiotic treatment.
Often there is a quick amelioration afterwards but in many cases this does not lead to a complete cure.
Instead we often see relapses of the problem - esp. with weatherchanges - over a period of months.
The term "Atypical pneumonia" emerged in the 1950ies out of the clinical finding that some cases of pneumonia did not respond curativly to the frequently used antibiotics. Lentze,2000

In cases of chronic (often recurrent) cough in children there we often find obstructive breathing right from the beginning and is often treated initially with inhalative steroids and other broncho-dilatators.

If oxygen-saturation sinks below 94% together with marked dyspnea and reduction of activity this shows often the transition of bronchitis into broncho-pneumonia. glt2] glt1,2,2023

Diagnostic pointers pew1,1904
The diagnosis of a lobular pneumonia, supervening as it does upon an existing diseased condition, is often difficult, especially in mild cases with a limited invasion.
The inflammation being limited to small and scattered areas of lung tissue surrounded by healthy lung tissue renders the detection of consolidation most difficult.
Thus one of the most reliable signs of the disease is not available, and for the same reason bronchial or broncho-vesicular breathing is not marked.
The physical signs are those of bronchitis with the added evidence of limited localized areas of consolidation.
The crepitant rale is a reliable sign, but is naturally masked in these cases by the moist rales of the co-existing bronchitis of the finer tubes.
From lobar pneumonia, broncho-pneumonia is distinguished by its bilateral and scattered development, the gradual onset, supervening upon another preceding disease, its lobular and not lobar character, and in adults by the mode of invasion.
From a rapid tuberculosis which it often resembles, the bacilli should be looked for, their presence or absence deciding the diagnosis.

Capillary bronchitis and broncho-pneumonia so nearly resemble each other clinically that some recent writers and teachers do not treat of them separately.
The clinical diagnosis between them is usually well-nigh impossible.
In simple capillary bronchitis the temperature runs a lower course as a rule, the prostration is more marked, defective aeration is very pronounced and we fail to find any areas of consolidation.
Capillary bronchitis, like broncho-pneumonia, is the result of an extension into the finer bronchioles of the inflammation starting in the larger tubes, but unlike catarrhal pneumonia there are not areas of consolidation nor the general aggravation of all the fever symptoms that mark the development of the latter.

Specifics on complications and sequalae pew1,1904

For general description of complications see chapter "Complications"

Pleurisy is a complication in many cases [...not as common as with lobar pneumonia, when it does occur there is a greater tendency in it to become purulent. bwax,1902], accounting for the respiratory pain, especially if the lobules involved are near the surface of the lung or the area of inflammation is extensive.
Diarrhea is a common complication in children and infants and is a serious factor.
Convulsions may occur and are of grave importance; in fact, the brain symptoms in severe cases may resemble those of Meningitis.
[Rolling of the head can be an initial symptom of meningeal irritation. glt2,2023]

[At times instead of the usual termination, suppuration and gangrene may result, or purulent collections may develop in the lung, surrounded by an area of congestion and inflammatory edema.
In other cases where resolution is slow, a proliferation of the connective tissue of the alveoli takes place, with a fibroid overgrowth of the septa, resulting in a contraction of the lung tissue which is known as Secondary Fibrinous Pneumonia. bwax,1902]

[Coughing after bronchitis/broncho-pneumonia is considered frequent and normal for the duration of up to 3 months and is not considered as a bronchial hyper-reactivity within this time period.
In children below 3 years of age with bronchial obstruction there is an increased risk of developing asthma, if at least one of the parents has an allergic disease or if there is continuous exposure to cigarette fumes. (cp. Schaub, Lentze, Pediatrics, Springer, 2003) glt1,2023]

Specifics in children gccx,1902

Note: Owing to the more embryonic condition of the child's lungs broncho-pneumonia in infants pursues a course in some respects so different from that in adults as to merit seperate description.
[Ed. See also the chapter on anatomic specifications in children]

Onset: Convulsions often replace or accompany the chill.

Skin: Is moist and perspiring.

Respiration: It is very rapid - from 40 to 80 per minute.

Nervous Symptoms: There is great restlessness and extreme prostration.

Pulse: It is usually very rapid, [in children above the age of 3 - soft, sometimes irregular, glt2] varying from 120 to 170 per minute or more.

Tongue: Early, it has a white, heavy coating, which later becomes brown and dry.

Gastro-Enteric Symptoms: The child takes nourishment with great difficulty.
There is sometimes vomiting.
In some cases there is diarrhea.

Urine: The urine is scanty and high colored.

Course and Duration: If the disease is extensive at the onset, involving a large number of lobules, with corresponding severity of the other symptoms, the case may end fatally in a few days.
In other cases, with mild onset, the case may be progressing favorably when suddenly, with extension of the disease into new areas, the temperature, from 100°F/37,8°C, may run up to 105°F/40,6°C or more within a few hours, and the case be rapidly fatal.
In severe cases the course of the disease is from one to two weeks.
Some cases persist, with irregular remissions and exacerbations, for six or eight weeks before convalescence begins.
[This sluggish process - also after antibiotic therapy - often leaves persisting residual infiltration, which can be reactivated with the next stress onto the system with a danger of diagnostic misinterpretation - esp. if there are months between the first pneumonia and the next episode of cough! glt2,2023]

In some cases cerebral symptoms predominate.
There may be great restlessness and delirium, interrupted by repeated convulsions.
The accompanying symptoms are: Rolling of the head; high fever; great prostration; vomiting; and other symptoms of meningitis.
Strumous Cases: In children with tuberculous diathesis the lungs become much congested; there is great prostration, high temperature, great loss of flesh, and swollen lymphatic glands.
Such a condition renders the prognosis grave.


Bronchiolitis

General Course

Etiology kroe1,2014
The term bronchiolitis is a collective term for various diseases, which differ from each other by partly very different etiology, histopathology, imaging and clinical symptoms as well as prognosis.
The causes of bronchiolitis are vary considerably.
Some possible examples are:: Chemicals or organic dusts or noxae (esp. chlorine, hydrochloric acid, sulphur dioxide and oxides of nitrogene), nicotine abuse, infections, drugs or collagenoses (e.g.: rheumatoid arthritis, Sjögren's syndrome).
In 80% of children's cases pathogenic agents like RS- and Adeno-virus or Mycoplasma are to be found,- but seldomly these agents are ever detected.
There are also forms with no apparent etiology (idiopathic).

The classification of bronchiolitis is difficult.
On the one hand, "bronchiolitis" is defined differently from pathological, physiological and clinical perspectives, emphasizing either morphological or functional aspects.
On the other hand, the term is associated with certain defined diseases such as obliterative bronchiolitis in chronic rejection after lung transplantation.
Furthermore, clinical classification is complicated by the loose association between the trigger, radiologic, and histologic findings.

Case-history kroe1,2014
A case-history relevant to bronchiolitis includes onset and duration of symptoms and any underlying disease (immunologic-hyperergic diseases, collagenoses) as well as questions regarding exposure to inhaled noxious agents (toxic gases, mineral dust, organic dusts, smoking), respiratory tract infections, medication use (D-penicillamine, gold, sirolimus), and transplantation.
Hereditary conditions (cystic fibrosis, primary ciliary dyskinesia) may also be indicative of bronchiolar disease.
In elderly, bedridden patients or with oropharyngeal dysphagia, chronic diffuse aspiration, bronchiolitis should be taken into consideration as a possible diagnosis.
Acute diffuse panbronchiolitis also occurs in perfectly healthy individuals in the setting of an infection.
Finally, the possibility of viral or Pneumocystis jiroveci-associated bronchiolitis should be considered if immunosuppression is present.

Symptoms gccx,1902
The symptoms of bronchiolitis, while related to those of bronchitis of the larger tubes, are so much more severe in degree as to make of the disease almost a distinct clinical picture.

The oncome of the attack is gradual when occuring by extension of a previously-existing bronchitis; in other cases, and in the greater number, the onset is sudden.

The initial chill may be a distinct rigor or repeated chills; in young children convulsions often replace the chill.

The range of temperature is usually high; soon after the onset it may rise to 103°F/39,4°C or 104° F/40°C or more, and the attack throughout may be characterized by this high temperature.
If the fever moderates, the invasion of new areas of lung tissue is announced by a sudden rise.
Towards the end, with cyanosis, the temperature falls and may even become subnormal.
[The Temperature is rarely above 101° - 103°F/38,3° - 39,4°C. bwax,1902]

The pulse is always rapid, varying according to the patient's condition form 130 to 150, and it may even be so rapid as to be uncountable.
It is of low tension, and sometimes so small as to be almost imperceptible.
[The pulse is 80 to 100 beats per minute. bwax,1902]

The cough is frequent, occurring often in paroxysms and attended by pain in the chest.
Early it may be dry, and in some cases remain so throughout the attack.
In the paroxysms of cough there is severe cyanosis.
With deep cyanosis and the approach of a fatal issue the cough subsides, owing to obtunding of the senses.

In some cases expectoration is absent throughout the attack; in others, it will be very scanty.
The sputum is viscid and expelled only after severe effort and cough.
In character the sputum - when present - is mucous; and later, it is muco-purulent.
The mass contains fine, short plugs, which are casts of the bronchioles.
These casts hang down under the lower surface of the mass when the expectorated matter is made to float on water.

The breathing is always rapid, and severe dyspnea is characteristic.
The number of respirations, according to the severity of the attack and the amount of lung tissue involved, will vary from 20 to 60 per minute, or, in extreme cases, the breathing becomes quick and panting; sometimes it goes on to asphyxia.
The respirations are short and quick, and aided by the muscles of respiration.
Orthopnea occurs early.
[The alae nasi are widely dilated, and expiratory dyspnea is extreme, often amounting to orthopnea early in the case. bwax,1902]

Skin: There is palor and a high degree of cyanosis.
The face is livid and the lips purple.
The skin is usually moist, sometimes even profuse sweat.
[There is a general perspiration, and the extremities are cold. bwax,1902]

Mind: Early there is much restlessness, [and anxiety is present from the start and may give place later to delirium bwax,1902] the patient is tossing about.
Later, as the blood becomes carbonized, there is lethargy, the patient showing great apathy; this may be accompanied by muttering delirium.
In fatal cases, near the end, there is usually coma.

[The digestive functions are impaired, the tongue is furred, and the bowels are constipated. bwax,1902]

Physical signs kroe1,2014
Clinical examination findings are also nonspecific.
Occasionally they find:
- Enlarged anterior-posterior thoracic diameter
- Hyposonorous palpitation (pulmonary hyperinflation with air trapping)
- Prolonged expiration glt2
- Expiratory wheezing (in case of obstruction) glt2
- Medium to coarse bubbly moist sidetone (in bronchiolo- or bronchiectasis)
- [In addition to the signs of bronchitis of the larger tubes there are heard, bilaterally, abundant sibilant rales which are replaced later by subcrepitant rales.] bwax,1902
- [The respiratory murmur is usually harsh and rough in the upper and anterior parts of the chest; at the bases and the back it is feeble]. gccx,1902
- [In children: Fine crepitant rales without further auxiliary sounds] glt2,2023

Diagnostic pointers kroe1,2014
The definitive diagnosis of this disease is difficult and includes history, physical examination, laboratory parameters, pulmonary function test, measurement of blood gases, HRCT and bronchoscopy.
The most important clinical parameters for the diagnosis of bronchiolitis are anamnesis (disease course and comorbidities) and HRCT patterns (direct and indirect signs).
Furthermore, broncho-alveolar lavage and transbronchial biopsy with histology can provide additional information.
One may possibly find an unremarkable pulmonary function or a mixed obstructive/restrictive ventilatory disorder in context with bronchiolitis.

Clinical signs of obstruction suggest constrictive bronchiolitis rather than hypersensitivity pneumonitis (EAA) or cryptogenic organistic pneumonia (COP)
[Since pathologic narrowing of peripheral airways is difficult to detect, these airways may be considered a "silent zone" of the lung.
Despite efforts to design tests to identify peripheral airway obstruction, none have been entirely successful.
More recently, higher recognition of the entities affecting peripheral airways and diagnostic advancements have increased the frequency of diagnosis.
Nevertheless, the epidemiology of disorders of the peripheral airways remains largely unknown.

Therefore definitive diagnosis of a specific bronchiolitis entity requires clinical, diagnostic (imaging, PFTs), and frequently, histopathologic evaluation.
Definitive diagnosis depends on excluding bronchial and alveolar involvement seen in alternative diagnoses.] mur1,2016

Specifics on complications glt1,2023
The most frequent complication is a hospital acquired super-infection.
Often following bronchiolitis a hyper-reactive state of the respiratory system develops over months with rhonchus in cold air without further signs of infectious disease.
Bronchiolitis obliterans (fibrinous cicatrization of bronchioli) is a life-threatening form/takes a life-threatening course.
It shows symptoms such as persisting wheezing, prolonged expiration sounds, low oxygen-saturation <90%, tachypnea and exertion in the final stages.
Orthodox therapy consists mostly of administering inhalatory steroids (often without major improvement) and oxygen.
This super-infection often occurs as a rejection reaction following bone marrow transplantation (esp. in children with leucemia).

Specifics in children glt1,2023

The disease in children is self-limitating within 10 days; often there is a spontaneous improvement on the third day.

Nurslings in their first months of life until the age of one show quickly arising tachypnoe (>50/min) as well as a rapid clouding of consciousness due to lack of oxygen.

In older children we see dyspnea following coryza, with massive spasmodic constriction, rhonchus, extended expiration, cough with inspiratory/expiratory moaning, wheezing.
Dyspnea and cyanosis predominate the classic picture.
The first warning sign is dyspnea, which makes eating and drinking impossible.
Oxygen-saturation quickly goes under 90%; hospitalization is required in 50% of the cases, because especially nurslings (under 1 year) are endangered of suffering apnoe and bradycardia!

Historical Remarks from around 1900
The course of the disease showed a sudden begin with high fever, full, soft pulse over 150/min, a short, dry cough ending in clouding of consciousness; dyspnea with breathing frequency of up to 60/min; cyanotic face; much restlessness and tossing about at the beginning of the disease.
The next symptoms were a rising level of carbone-dioxide in the blood, lethargy, murmuring delirium passing over to coma.

Striking features on auscultation were: Sharp bronchial obstructive sounds in the thorax, rhonchi sibilantes, reduction of breathing sounds at the base of the lungs with crepitation.
Paradox breathing was often described with spasmodic constrictions mainly of the fossa subclavicularis.

In children under 1 year of age bronchiolitis often ended lethally within 24 hours, older children had a crisis at day 4-5, if they overcame this, they survived with improvement of all symptoms after one week.

Fatal progression was frequent in children with congenital heart- and kidney-diseases/-complications or miliary tuberculosis.

[At that time the disease mainly occured in malnurished nurslings, children with rickets or following whooping-cough, measles or influenza.] gccx,1902


Varieties of Pneumonia

Epidemic Pneumonia Ed.

This often shows peculiarities as every epidemic disease does.
The specifics can vary from one region to another and usually change every year.
In one epidemic with pneumonia typhoid symptoms may be prominent, in another heart complications, cerebral or gastro-intestinal features, etc.
Pathogenes which lead to such epidemics more often are, for example, influenza-viruses (app. every 40 years a peak win1,2021), measles, corona-viruses and others.
The treatment can be management according to Hahnemanns' instructions in the Organon (6th edition - §100-102) on how to treat epidemic diseases.

Atypical pneumonia mur1,2016

Definition:
The syndrome of gradual onset of fever, non-productive cough, and a relatively normal white blood cell count in a patient without a readily demonstrable bacterial pathogen has been called "atypical pneumonia".
Frequently systemic complaints are more prominent than the respiratory ones.
The atypical syndrome is characteristic of infections by pathogens such as Mycoplasma pneumoniae, Chlamydia species, C. burnetii and viruses (Ed.: or multi-resistent coccus-bacteria!).
However, several studies, including one that included patients with mild CAP treated on an outpatient basis, have found that neither the clinical symptoms nor the radiographic manifestations are sufficiently sensitive or specific to guide pathogen-directed antibiotic treatment against "typical" versus "atypical" microorganisms.
Therefore, current guidelines do not emphasize the use of the typical versus atypical classification to determine initial empirical antibiotic treatment for CAP.

Editors:
What makes a pneumonia an "atypical pneumonia" is defined by the symptoms and the course of the disease NOT by the infectious agents involved! In our opinion Atypical pneumonia is a spectrum of cases which cannot be assigned to one of the other standard forms of pneumonia (e.g. lobar pneumonia, broncho-pneumonia, etc.) can have a gradual but also quick onset.
To us many (but not all) cases seem to fit the definition of Galic below.
Important to us seems the possible connection to multi-resistant hospital-acquired "atypical pneumonias" because this is a major threat with HAP worldwide!

[Diagnostic pointer: If legionellosis or a chlamydial infection is suspected, serum transaminases and alkaline phosphatase should also be determined.] ebm1,2015

The incidence of pleural effusions with so-called primary atypical pneumonia (usually caused by Mycoplasma or viruses) is as high as 20%.
The effusions associated with atypical pneumonia are usually small, are exudative, and contain predominantly neutrophils.
If there is sufficient fluid, as described earlier, thoracentesis should be performed to exclude a complicated parapneumonic effusion.

Clinical additions glt2,2023:
Typically Atypical pneumonia occurs during the cold time of the year, especially in wet cold weather, often taking an epidemic course.
The general condition is often worse than the local findings with profound exhaustion for weeks, uncharacteristic headache, pain in joints or limbs.
Fever is often around 38°C/100,4°F (often without chill) or patients are without fever, with copious night sweats.
Often we see a tendency towards asthmatic breathing, aggravation wet-cold weather.
[We see patients in general bad condition (e.g. pale, weak, no appetite, emotionally unstable, asthmatic breathing) but with little characteristic symptoms with frequent and torpid relapses.] glt2

On auscultation with these interstitial pneumonias you find pronounced bronchial breathing and often no crepitation.
[Often these pneumonias are (worse) on the left side.
These pneumonias often start from the center - in these cases you cannot hear any pathological findings on auscultation. glt2] Take care: A negative finding on physical examination does not rule out an atypical pneumonia! Therefor in case of doubt always do an x-ray!

[On X-ray we often only see persistent peribronchial, interstitial small-spotted infiltration, or peribronchial stripes, not more.] glt2

O2-saturation is often between 92-94%.
On an x-ray you often find profuse shadowing, which frequently is much more extended than the auscultational findings would indicate.
Blood-findings: normal or reduced leucocyt-counts, potentially developing into a relative lymphocytosis.
Possible complications are septic dissemination of infectious agents resulting in otitis, meningitis, brain-abscess or endocarditis.
Especially in immune-suppressed patients atypical pneumonias are frequent and often - corresponding with the severity of the chronic state - end lethally.
Aged persons more often show an atypical course of disease! [In western countries like Germany I have the impression of 15-20% atypical forms - in young people between 5 and 20 years of age these atypical pneumonias seem to me already 30-40%!] glt2

[Common laboratory-blood-findings for infection (like leucoctye-counts, differential bood-counts, CRP) often show no corresponding results.] glt2

From a holistic-medical point of view it seems interesting, that in the pre-antibiotic era cases of atypical pneumonia were seldom and only observed in aged people.
In modern scientific literature these cases take up more and more space due to continually newly arising infectious agents demanding continually more complex (orthodox) medication.

Frequently antibiotic therapy fails here.
Many patients still feel weak after treatment, cough and dyspnea persist for 30 days up to several months.
[Beside the fitting antibiotic therapy, ambroxol seems to play an important role in orthodox medical treatment.
Very often these infections are treated for a too short duration (12 weeks of antibiotic treatment are at least needed).
Corticoid therapy often palliates for a short time but in the end it aggravates the whole infectious condition.
Often these cases leave the patient in an asthmatic state triggered by allergens and infection (esp. if there is a family history of allergic disease!).
But behind this allergic immune-response is this badly treated atypical pneumonia. glt2] In this case patients are often treated with asthma-medication instead of anti-infectious therapy.
[Homeopathically many conscientiously choosen remedies fail to help sustainably, nosodes like Tub. tend to aggravate.
In these cases we found the old repertory-rubric from JT Kent "Chest/Tuberculosis/Sycotic" a valuable rubric to start with the search for help (Ed.: In this book in the repertory under Pneumonia/Atypical pneumonia).
Also the rubric Pneumonia/Neglected can help in the search for a curative remedy.] glt2

Editors: See also the definition-hypothesis in the glossary for "Sycotic tuberculosis".

Tuberculosis

Former synomys: Phtisis, Consumption, Scrofula
Tuberculosis used to be one of the most common causes for pulmonary inflammation and the most life-threatening one world-wide.
Yet in modern terminology it is treated as a completely independent disease entity.
Therefore we thought it worthwhile to give a little insight on tuberculosis in the context of pneumonia.
Further information is given in the chapter "Differential diagnosis" (See p. XXX)

History
For a long time tuberculosis had gone undetected, masked by various diseases such as phtisis, pulmonary consumption, scrofula, lupus (phagedenic lichen), caries of the bones.
Only after Robert Koch had discovered the tubercle bacteria in 1882, could it be proved without any doubt that all these diseases, such as tuberculosis of the joints, tuberculosis of the bones, tuberculosis of the kidneys, scrofula, lupus etc. are caused by the same pathogens. win1,2021

Epidemiology
Tuberculosis was and is the most common life-threatening bacterial infectious disease worldwide (cp. Chapter Epidemiology).
One third of the world's population is infected; an estimated 60 million people suffer from open tuberculosis.
Eight to ten million new cases are added each year, and three million people die of this disease annually.
These staggering numbers mainly affect the developing countries of Africa, Asia and South America.
It is to be feared that in the last decade of this millennium more than 20 million people will die of tuberculosis, mainly in connection with HIV-infection. win1,2021

One hundred years ago, one in seven adults in Central Europe died from chronic tuberculosis.
It was not until the middle of the 20th century, when the hygienic conditions improved sustainably, the BCG vaccination [Bacille Calmette Guerin = attenuated bovine strain; named after the french developers Ed.] became available as a preventive measure, and new effective tuberculostatics were discovered as a therapeutic measure, that the once devastating epidemic was considered to be under control, at least in western industrialized countries. win1,2021

In particular, the improvement of hygienic measures, such as the abolition of the formerly customary spitting of saliva and ritual kissing of religious relics, have been instrumental in reducing the spread of pathogens.
In addition, the reduction of hunger and the improvement of housing conditions have drastically improved the population's general immunity. Ed.

In tuberculosis we differentiate between two main reservoirs of infection: openly tuberculous humans as the most important carriers of Mycobacterium tuberculosis and diseased and bacteria-excreting cattle as the almost exclusive carriers of Mycobacterium bovis.
Due to the consequent eradication of tuberculous cattle, infection with Mycobacterium bovis - e.g. through the consumption of raw milk - is almost non-existent in industrialized countries. win1,2021

In the 19th and early 20th century, cattle suffering from tuberculosis were not rare also in industrialized countries.
About every 3rd dairy cow was infected and could therefore contribute to the spread of Mycobaterium bovinum.
Mycobacterium bovinum was frequently detected in lymphatic tuberculosis (formerly scrofula).
It can therefore be assumed that the so-called "scrofulosis" had spread mainly through milk containing the pathogen.
Pulmonary tuberculosis, however, was more likely to be spread by droplet infection. Ed.

Transmission of M. tuberculosis is influenced by features of the source case, particularly the bacillary load, by the closeness of the potential recipient of the organism to the source, and by the condition of the environmental air they share.
A possible additional factor is the infectivity of the organism, the degree to which M. tuberculosis has the ability to establish itself within the lungs or other sites in the new host.
However, even taking these factors into account there is substantial unexplained variability in the degree to which persons with untreated tuberculosis transmit the infection to persons to whom they are exposed. mur1,2016

Pathology
The genesis of the pathologic reactions in tuberculosis is inextricably linked with the response of the host to the invading tubercle bacillus.
In most individuals infected with M. tuberculosis, the host response - innate and adaptive - restricts the growth of the pathogen, thereby containing the infection.
Paradoxically, however, the immunologic response to M. tuberculosis is likely responsible for the characteristic presentation of tuberculosis.
In contrast, the near absence of cell-mediated adaptive immunity in patients with advanced HIV (human immunodeficiency virus) infection is assumed to be responsible for the atypical presentations of tuberculosis in HIV-infected patients.
Such patients tend to have multisystem involvement and tend not to have cavitary lung lesions.
Although the lack of immune response minimizes tissue damage, the organism is not met with an effective protective response, thus facilitating proliferation and dissemination of the bacilli. mur1,2016

In ninety percent of all those infected for the first time, the primary complex heals spontaneously as the tubercles are encapsulated and calcify.
After the initial infection, antibodies are formed which protect the organism against further spreading of the disease and also against newly invading tubercle bacilli.
The presence of these antibodies can be tested with Tuberkulin (a substance obtained from tubercle bacilli) by skin testing. win1,2021

If necrosis and melting of the lung tissue occur in the post-primary stage in a calcified focus in which tubercle bacteria survived, a cavity, a cavern, is formed, which offers an ideal breeding ground for tubercle bacteria.
Cavity carriers are particularly dangerous to their environment because they are always to be considered "open".
Each coughing bout can be dangerous to the environment, since the carrier can spread TBC by droplet infection.
This post-primary tuberculosis after reactivation of an endogenous foci is the typical form of adult tuberculosis.
The vast majority of cases (over 85%), are pulmonary tuberculosis. win1,2021

Complications
If cellular immunity is insufficient, primary tuberculosis may progress to miliary tuberculosis within a few months of infection.
Seeding is lymphogenic or hematogenic.
Young children are particularly affected, with numerous small lesions of milium grain size (milium = millet grain) developing in the affected organs (lungs or meninges). win1,2021

Tuberculosis can cause very extensive complications due to its easy chronification and distribution throughout the organism.
We distinguish between the following forms: lympahtic-, genito-urinary-, bone and joints-, central nervous system-, abdominal-, pericardial-tuberculosis.

In 2012 in the United States, 21% of newly reported cases of tuberculosis involved extrapulmonary sites only and an additional 10% involved both pulmonary and extrapulmonary sites.
The proportion of patients with extrapulmonary involvement is greater among patients with HIV infection.
In one large retrospective study of tuberculosis in patients with HIV infection, approximately one third of the patients had only extrapulmonary sites of involvement, one third had both pulmonary and extrapulmonary disease, and one third had only pulmonary involvement. mur1,2016

Tuberculous lymphadenitis usually presents as painless swelling of one or more lymph nodes.
The nodes most commonly involved are those of the posterior or anterior cervical chain or those in the supraclavicular fossa.
Frequently the process is bilateral, and other noncontiguous groups of nodes can be involved.
At least initially, the nodes are discrete and the overlying skin is normal.
With ongoing disease, the nodes may become matted and the overlying skin inflamed.
Rupture of the node can result in formation of a sinus tract, which may persist for years.
Intrathoracic adenopathy may compress bronchi, causing atelectasis, thereby leading to lung infection and perhaps bronchiectasis.
Although rare, upper airway obstruction may result from cervical node enlargement.
Both chylous pleural effusion and ascites have resulted from intrathoracic or abdominal node involvement with obstruction of retroperitoneal lymphatics or the thoracic duct.
Tuberculous lymphadenitis may also appear or worsen as a manifestation of IRIS (immune reconstitution inflammatory syndrome; it's a syndrome that occurs during antiretroviral therapy of HIV during tuberculosis and vice versa).
The diagnosis of tuberculous lymphadenopathy is established by lymph node biopsy or aspiration with histologic examination. mur1,2016

Current Problems
In children, BCG has been demonstrated to prevent disseminated and miliary tuberculosis and tuberculosis meningitis.
In adults, the results of BCG vaccination are less clear; of eight controlled clinical trials of BCG against pulmonary tuberculosis in adults, protection has ranged from 0 to 70%. mur1,2016
Interestingly, when two different vaccines were used in a Medical Research Council Trial in the United Kingdom, one of which produced only poor TST (tuberculin skin test) reactivity, equal degrees of protection were seen.
Conversely, no protection was seen in the South Indian Trial of more than 200,000 people monitored for 15 years, although all patients who developed tuberculosis had been converted to TST positivity by the vaccine.
It is unclear why BCG appears to be effective in some parts of the world and not in others (a finding that is also evident in protection against leprosy).
Clearly, there is a great deal yet to learn about the nature of protective host immune responses, host genetic factors, variations in pathogenicity of tubercle bacilli, and the role of exposure to environmental nontuberculous mycobacteria that may provide resistance or enhance susceptibility. mur1,2016

A recent clinical trial demonstrated that a novel tuberculosis vaccine termed MVA85A induced the expected immune responses but failed to protect against tuberculosis when used to boost BCG vaccine in infants; such results again demonstrate that improved understanding of tuberculosis pathogenesis and protective immunity are needed to inform development of efficacious vaccines.
We are still far from understanding why the natural immune system (which prevents 90% of persons infected from developing active tuberculosis) fails in 10% of those infected and why the adaptive immune response in tuberculosis does not protect us from repeated infections.
In spite of these gaps in knowledge, several additional vaccine candidates are now being tested. mur1,2016

Tuberculosis is becoming a more complicated disease globally because of the appearance of MDR (multi drug resistant) and XDR (extensively drug resistant) organisms and the increasing frequency of comorbidities, particularly HIV infection but also other risk-enhancing factors such as diabetes, renal insufficiency, immunosuppressive drugs, and tobacco and other substance addiction.
Clearly, new diagnostic tools and therapeutic options are urgently needed.
Currently, the most extensively used diagnostic methods around the world, both for active tuberculosis (sputum smear microscopy) and for latent tuberculosis (TST), were invented at the end of the 19th century.
Similarly, BCG vaccine, despite its wide use, does not provide the needed protection.
Today's standard treatment with four drugs (isoniazid, rifampin, ethambutol, and pyrazinamide) has remained unchanged for more than 30 years, must be taken for a minimum of 6 months, and is insufficient to treat patients with MDR or XDR tuberculosis. mur1,2016

Homeopathic Treatment Ed.
Homeopathic treatment has a very long tradition also regarding tuberculosis and can certainly be considered to be an option for attempting to cure this disease.
Especially since problems are increasing within the orthodox medical approach, as described above.
Whether this publication will also be helpful for treating an acute pulmonary tuberculosis (as a special form of pneumonia), experience will show.
The opinion of the authors is that if the symptoms correspond to those described in the Materia Medica and the Repertory, the homeopathically selected remedy will help regardless of the name of the causative agent.
We editors hope that somebody will collect and integrate all of the 200 years of homeopathic experience in treating people with tuberculosis, as we have accomplished in this publication regarding pneumonia.

Influenza and Influenza-like-disease (ILD)

Former synomys: La Grippe, catarrhal fever

History
Influenza epi- and pandemics can be traced back to ancient times.
There have been many different names, pathological theories, and forms of medical treatment throughout Europe.
The principle of contagion was theoretically recognized early on, although spreading was attributed to the wind and weather or to superstitious and religious reasons.
Due to the long-lasting theory of humoral pathology until the end of the 19th Century, sweat cures and bloodletting were common and sometimes more deadly than the disease itself.
Hygienic practices were also virtually unknown in the Middle Ages.
The handkerchief, for example, had not been developed until the 16th century, and was largely rejected by the population. Ed.

At the end of a severe influenza epidemic (1889-1892), Richard Pfeiffer (1885-1945), a student of Robert Koch, found small, delicate rods that grew only on blood-containing culture medium in the sputum of influenza patients.
Pfeiffer was convinced that he had discovered the actual pathogens in these "hemophilic rods".
[Later, these rods were called "hemophilus influenzae." Ed.]
In 1933 the English researchers Smith, Andrews, and Laidlaw provided the final proof that a virus is the etiological factor causing human influenza.
Three types of virus were identified: type A, type B, and type C.
Since then, only the type A influenza virus has been identified in pandemics and major epidemics.
The strong variability of the two surface subtype antigens H (hemagglutinin) and N (neuraminidase) of the influenza virus type A leads to numerous subtypes.
Unlike other viral infections such as smallpox, yellow fever, poliomyelitis, measles, and rubella, comprehensive vaccine protection cannot be achieved because of the variability of surface antigens of the type A influenza virus.
Due to gene replacement, domestic animals (poultry and pigs) may play an important role as virus reservoirs in genetic recombination.
It is considered certain that such new virus subtypes emanate new influenza pandemics from time to time, when human and animal viruses merge, forming a new combination.
These pandemics give the impression of secular ripples and occur in a rhythm of about 20-40 years. wink,2013

SPANISH INFLUENZA Ed. [Summary of pkx2 and wink,2013]
[In 1918, toward the end of World War I, the most severe influenza pandemic to date occurred, lasting until 1923 with minor interruptions.
This pandemic affected 700 million people. wink,2013]
In three waves it killed approximately 20 to 50 million people out of a world population at the time of approximately 1.7 billion.
The circumstances leading up to the pandemic at the time were unique and most likely responsible for the high lethality, especially among young adults under 40, and are not yet fully understood in their entirety.
Until Nov. 11, 1918, World War I raged, resulting in hunger and lack of resources, also medical supplies and medical staff.
Many cases of influenza were diagnosed, but numerous incorrect diagnoses were also made at the time: cholera, appendicitis, chlorine gas poisoning, epidemic typhus, scarlet fever, three-day fever, and even a form of "black death" (plague).
It was not until 1951 that the H1N1 influenza virus of the Spanish flu was finally isolated from corpses found in the permafrost of Alaska.
Since the disease was not known, the recommendations of the medical profession were limited.
In addition to recommendations on hygiene (e.g., sneezing into a handkerchief, mouth-nose coverings), numerous medications such as aspirin, quinine, opium, heroin, alcohol, digitalis, and strychnine were used.
Aspirin, which was developed in 1897, was modern at the time and was used very frequently.
The drug had the special significance of being able to cause Reye's syndrome in young patients, especially in connection with H1N1.
This is a disorder of the mitochondria which can cause encephalopathy and fatty degeneration of internal organs, especially of the liver.
The specific symptoms such as delirium, bloody sputum, and hyperventilation strongly suggest the "Spanish Lady".
Today, [Because of its possible association with Reye's syndrome, aspirin must be avoided for pediatric patients. mur1,2016]
Even today, the full-blown Reye's syndrome has a lethality of 75% despite intensive medical treatment.
There are reports according to which high-quality homeopathic care has a significantly lower lethality of 1-2% in contrast to approx. 30% of the former orthodox medical treatment and to poor quality homeopathic treatment.

INFLUENZA-LIKE ILLNESS mur1,2016
Viral infections are important causes of disease of the respiratory tract.
The common cold is the most frequently encountered infectious syndrome of humans, while influenza continues to be a major cause of mortality and serious morbidity worldwide.
Respiratory viral infections frequently complicate the course of patients with chronic obstructive pulmonary disease (COPD) and asthma.

The clinical syndrome of influenza is characterized by the rapid onset of general symptoms, including fever, chills, prostration, muscle ache, and headache, concurrent with or followed by upper and lower respiratory tract symptoms.
Systemic symptoms tend to dominate for the first several days of illness, whereas respiratory complaints, particularly cough, predominate later in the first week of illness.
Photophobia, excess tearing, and pain with eye movement are common early in the illness.
Mild conjunctivitis, clear nasal discharge without obstruction, pharyngeal injection, and small tender cervical lymph nodes are frequently present.
Fever may peak at 39° C to 40° C or higher and can last for 1 to 5 days.
Persistent nonproductive cough, easy fatigability, and asthenia are common in the second week of illness.

Influenza type A and B viruses are the most important causes of the influenza syndrome, particularly when the illness presents in an epidemic form.
However, the syndrome can also be seen in association with infection by other viruses, including adenovirus, parainfluenza, and RSV.

TRANSMISSION mur1,2016
The routes by which the different respiratory viruses spread from person to person are variable and include combinations of contact, droplet, and aerosol transmission.
For example, rhinovirus and respiratory syncytial virus (RSV) are primarily spread by direct contact with contaminated skin and environmental surfaces followed by self-inoculation of virus onto the nasal mucosa or conjunctiva.
Other viruses, such as measles and varicella-zoster viruses, spread as small-particle aerosols.
Other viruses may spread by means of larger-particle aerosols over short distances (1 m).
The relative importance of the various transmission routes under natural conditions for each virus varies and in many cases is unknown.

PATHOGENESIS OF INFECTION mur1,2016
The initial sites of infection and pathogenesis differ for the various virus groups.
Some, such as rhinovirus, are associated mainly with upper respiratory tract involvement.
Others, such as influenza, commonly invade the lower airways and sometimes pulmonary parenchyma in addition to causing upper airway disease.
The viruses also differ in the relative contributions to the clinical manifestations of disease from damage due to direct viral mechanisms and damage due to host immune responses and inflammation.
An additional important feature of respiratory virus infections is their effect on the resident bacterial flora of the upper airways.
Respiratory virus infections alter bacterial colonization patterns, increase bacterial adhesion to respiratory epithelium, and reduce mucociliary clearance and phagocytosis.
These impairments of host defenses by viruses allow colonization by pathogenic bacteria and invasion of normally sterile areas, such as the paranasal sinuses, middle ear, and lower respiratory tract, resulting in secondary infection.

COMPLICATIONS
Typical complications are otitis media, tonsillitis and further complications such as peritonsillar abscess, chronic bronchitis, bronchiolitis, pneumonia, ARDS (acute respiratory distress syndrom), MIS (Multisystem Inflammatory Syndrom) and septic conditions. Ed.

BRONCHIOLITIS mur1,2016
The majority of cases in which an etiologic agent has been identified are associated with RSV.
Other viruses associated with bronchiolitis include human metapneumovirus, bocavirus, parainfluenza virus, influenza A and B viruses, adenovirus, measles, and rhinoviruses.
The major differential diagnostic consideration is asthma, which is uncommon in children younger than one year old.

PNEUMONIA mur1,2016
Viruses are important causes of pneumonia in both adults and children.
They have been associated with up to 40% of radiographically proven pneumonias in hospitalized adults and are estimated to cause 16% of total pneumonias in pediatric outpatients and up to 49% in hospitalized infants.
These figures may underestimate the importance of viral infections as a cause of pneumonia, particularly in outpatients, because of the insensitivity of viral diagnostic methods and because of the lack of chest radiographs in many patients with acute viral infections.

The relative importance of the different viruses as causes of pneumonia depends on the season and the age distribution of the population under study.
During outbreaks, influenza virus accounts for more than 50% of viral pneumonia in adults.
In addition, RSV, adenovirus, parainfluenza virus, and varicella virus cause pneumonia in normal adults.
Unusual viruses continue to emerge in epidemics of severe acute pneumonitis, including hantavirus, coronavirus (SARS), and avian influenza A viruses.

In children, RSV, parainfluenza virus, and adenovirus, in addition to influenza viruses, are the most important causes of pneumonia.
Measles virus pneumonia affects children and adults during epidemics in susceptible populations.
There are reports of cases of pneumonia in adults and children attributable to rhinovirus, but the evidence that these viruses are definite causes of pneumonia is circumstantial.

The clinical and radiographic features of sporadic cases of viral pneumonia are usually not sufficiently characteristic to permit specific viral diagnosis or differentiation from bacterial pneumonias on clinical grounds alone.
Exceptions include measles and varicella pneumonia, in which the associated rash establishes the diagnosis.

Therefore, attention is first directed at excluding primary or secondary bacterial pneumonia.
Tests to detect viral antigens or nucleic acid are increasingly available and are rapidly being adopted as the preferred approaches for establishing the etiologic diagnosis.

Viral pneumonias with extensive involvement of lung tissue may require prolonged ventilatory assistance and pulmonary rehabilitation.
Some cases of viral pneumonia have a rapid and relentless fatal course, with generalized alveolar and interstitial opacities, development of the adult respiratory distress syndrome (ARDS), and progressive respiratory failure.

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