Recent Contributions to the Study of Pyelitis in Infancy

American Journal of Diseases of Children, Volume XII: Pages 235-243, September 1916.

Progress in Pediatrics


The term pyelitis is used to designate an acute febrile disease characterized by the presence of pus in the urine. Brennemann1 estimates that these cases constitute 1 per cent, of all those coming to a physician. The symptoms are usually abrupt in onset, the temperature often reaches 103 or 104 F. The fever may be relapsing in type2 extending over variable periods of time, sometimes simulating malaria.3 Rigor may be present and is almost pathognomonic of this disease when it occurs in infants under 2 years of age.1-4 The nervous symptoms may suggest meningitis.4 Sometimes there are definite symptoms pointing to the genito-urinary tract, as frequent micturition accompanied by more or less pain,4-5 but more frequently there is nothing to indicate any disturbance in these parts.1 The physical examination is usually negative except that pallor is characteristically present.1 In some instances the kidney is palpable,1 more often the right than the left, and often the spleen is palpable at the onset of the disease.4 There may be tenderness in the lower abdomen.4 or back, which makes the patient object to being handled.1 Occasionally there is pain and tenderness of the joints with signs of local inflammation.4 Herpes may be present.4 Occasionally there is an inflammatory condition of the vulva.4

Urine : A single specimen of urine may be normal. The sediment may contain only bacteria,7 but usually shows also many leukocytes. The urine may be opalescent, due to the presence of microorganisms.4,8 The reaction is acid when fresh, but becomes alkaline on standing.9 The amount of albumin is slight.6 The presence of casts indicates that the parenchyma of the kidney is involved, but their absence does not necessarily mean that the kidney is normal.4 Pus may be temporarily absent from the urine when only one kidney is diseased, due to a blocking of the ureter.1-9 The organisms responsible for the infection are colon bacilli in a very large percentage of the cases.9 Jeffries10 reports 121 cases, 67 colon, 37 staphylocoeci, 10 streptococci, 3 pneumococci and 4 miscellaneous. The colon bacilli when present are extracellular and show a tendency to beading.1,6


The course of the disease is very variable. Usually the acute symptoms are over in a few weeks. A considerable number of cases tend to become chronic and may last for years with acute exacerbations. Birk11 reports one child who had five recurrences in ten years, the last at the age of 12. Not infrequently the acute attacks come in storms with periods of comparative health between.12 Some infants have attacks like periodic vomiting and may pass into coma.4 The ultimate outlook in nearly all cases is favorable, but the rapidity of the cure depends largely on one's definition of "cured." The more favorable statistics come from those who do not require that the urine be culturally free from bacteria before calling the patient cured. Thompson8 believes that chronic interstitial nephritis may result because of the slow infection of the kidney by colonbacilli.


Pathologically two types of the disease may be distinguished.1 The first shows simply a catarrhal condition of the bladder and the pelvis of the kidney. The second, which occurs especially in children with low resistance, shows multiple abscesses in the cortex of the kidney.13 Most of the autopsies are in this type. Sometimes these abscesses radiate toward the pelvis in fine lines.The bursting of these abscesses gives rise to pyuria.8 Müller14 believes that the infection from the pelvis of the kidney in these cases travels by way of the lymphatics and that the tubercles play a secondary rôle. Very few autopsies have been made, because the condition is so rarely fatal. Apparently no permanent damage to the kidney results in cases which are cured. Friedenwald15 reports one case in which the patient died of tuberculosis seven weeks after a cure of pyelitis and there were no lesions in the genito-urinary tract.


The diagnosis of pyelitis can be made only by an examination of the urine. Agglutination reactions and opsonic index determinations are of no value.6


The mode of infection has been the subject of much controversy. Birk11 believes that a coexisting tuberculosis and the so-called exudative diathesis are predisposing factors. Brennemann1 has called attention to the fact that it occurs more frequently in the summer months. Friedenwald15 showed that fifty-nine out of eighty cases had preceding gastrointestinal disturbances. Very frequently cases are preceded by acute nasopharyngeal infections.

The fact that such a very large percentage of cases occur in girls has given support to the theory of an ascending infection. The disease is most common in the diaper age, when there is great possibility of contamination of the urethra with fecal matter. Against this mode of infection has been cited the fact that rarely is there any cystitis present in these cases and that in vulvovaginitis of infants cystitis is rare.16 Leutscher17 has shown that bacilli may be present in the bladder without a cystitis, so that an infection of the kidney might occur. Dudgeon6 has also reported twenty cases of constipation, two of which had colon bacilli and pus in the urine, but no cystitis or other constitutional symptoms. The disease occurs in boys following circumcision, which is taken to indicate an ascending infection.18 It is possible, as Thompson9 has pointed out, that the infection is ascending, but the lumen of the ureter is less important than the deep tissues around it and around the urethra. Stewart19 has shown experimentally that the vessels of the ureter usually carry infection, not the ureter itself.

Another theory of the mode of infection is that the bacteria are borne to the kidney by the blood-stream. Presumably the bacteria enter the blood-stream from the intestines or possibly through some break in continuity of tissue about the rectum. In order that these bacteria shall do harm there must be a lowered resistance of the kidney or an injury to the tissues of the kidney, but this injury may be caused by the toxins liberated from the bacteria in the blood.13 Apparently certain healthy persons take bacilli coli from the intestines and excrete them through the kidneys.5 The number and virulence of these organisms depends on the intestinal condition. Anything which interferes with free excretion of the urine tends to produce an infection of the kidney. Experimentally it is possible in certain instances for the bladder to become infected by this means and the kidney itself remain normal.21

A third possible mode of infection is the direct transmission of bacteria from the intestines to the kidney. Probably this does not occur unless there is some damage to the lumen of the intestine.13 It has been shown21 in rabbits that the ascending colon and cecum are connected with the right kidney by a chain of lymphatics. None are found connecting with the left kidney. If only one kidney is affected by infection it is more frequently the right.10 With even a slight damage to the intestinal wall, bacteria can pass by the lymphatics directly into the kidney. There is also a free anastomosis between the lymphatics on the side of the vertebral column and those of the ureter so that an infection might easily occur from some outside source.22

The consensus of opinion seems to be in favor of the ascending method of infection in the majority of the infants under 2 years of age. The condition in these cases is rarely anything more than a catarrhal pyelitis. In children beyond 2 years of age the other means of infection come into play and not infrequently the severer types of lesions with multiple abscesses are found.


Spontaneous cure occurs in many acute cases.23 Many of the chronic cases are resistant to all means of treatment. Box4 says the value of any treatment is to be measured by its action in chronic cases. In the acute cases there seems to be the greatest uniformity in the belief that the urine should be made alkaline and kept so for a considerable period of time, and that free diuresis should be established.24 Colon bacilli are believed to develop less easily in an alkaline urine and phagocytosis of the bacilli by the leukocytes is more active in an alkaline medium.25 Potassium citrate or sodium bicarbonate are the drugs most used in this connection. Directly opposed to this view is the observation of Betz,26 that the thin, weakly acid urine occurring normally in pyelitis is the most favorable culture medium for the colon bacillus, but that it is unable to proliferate in very acid concentrated urine. He gives phosphoric acid and a meat and no-vegetable diet in order to make the urine strongly acid, and limits the intake of fluids and gives hot air baths to produce concentration.

The statements in regard to urinary antiseptics would make one feel that on the whole they are not of great value in the acute cases and worthless in the chronic cases. Ammonium and sodium benzoates,24 calomel,12 sandalwood oil,24 creosote,27 salol15 and urotropin are among the drugs recommended. Hexamethylenamin, combined with a sodium salt is said to be more efficacious than the simple hexamethylenamin.28 The colon bacillus easily becomes accustomed to any drug given internally, so a change of drugs should be made frequently.26 Nevertheless, hexamethylenamin is the favorite antiseptic drug. In this connection it is important to bear in mind that the action of hexamethylenamin depends on its being broken up in the body and excreted as formaldehyd. Sisson29 and others have shown that the excretion of formaldehyd takes place only in an acid urine. It has been customary to give hexamethylenamin in connection with alkalies, and this may account for the unsatisfactory results from its use. Thompson recommends that it should be given always with an equal amount of sodium benzoate.8 Box4 has shown that hexamethylenamin has very little influence on the colon bacillus, and Dudgeon6 goes so far as to say that if a patient with pyelitis is benefited by hexamethylenamin, the offending organism is not a colonorganism.

Vaccines in the acute and subacute cases do not appear to influence the result obtained by other methods of treatment.4,12,24,30 They are of no value in chronic cases. Vaccines do not prevent exacerbations, nor affect the presence of pus and blood in the urine.31 In some cases they apparently give relief of symptoms.32-35 Lyman says36 that autogenous vaccines are of great value, but adds, "many cases do not improve more rapidly than others without it." Rolleston reports favorably on their use.18 Dick25 believes that cases which do not respond to alkaline diuresis are sometimes benefited by vaccines. Serum apparently has no bactericidal action on the colon bacillus. Normal human serum and immune horse-serum are identical in this respect.6

Pardoe24 suggests that in the chronic cases there is possibly some underlying condition, as a disturbance of the gastro-intestinal tract, which must be relieved before the pyelitis will subside. Free evacuation of the bowels is advocated,27 and the giving of calomel and cold enemas.12 Some longstanding chronic eases of bacilluria are entirely cured by appendectomy, even though there are no symptoms referable to that organ.8,30 Operation is advised in cases in which there is any suggestion of abdominal disease or in those very stubborn to treatment.10 No local treatment is indicated in acute cases. In resistant chronic cases bladder washings with various antiseptic drugs may be tried.24 Koll37 believes that the best results are obtained by the use of aluminum acetate.

329 Beacon Street.


  1. Brennemann: Jour. Amer. Med. Assn., 1911, lvi, 631.
  2. Wassermann: Am. Jour. Med. Sc., 1911, cxliii, 878.
  3. Vanderhoof: Jour. Am. Med. Assn., 1912, lviii, 1172.
  4. Box: Brit. Med. Jour., 1910, ii, 1128. [Full Text]
  5. Rawls: Med. Rec., New York., 1911, lxxx, 709; Med. Rec., New York, 1912, lxxxi, 359.
  6. Dudgeon: Lancet, London, 1908, i, 615.
  7. Porter and Fleischner: Arch. Pediat., 1910, xxvi, 826.
  8. Thompson, W. H.: Med. Rec., New York, 1910, lvii,
  9. Thompson, T.: Quart. Jour. Med., 1909-10, iii, 251.
  10. Jeffreys, W. M.: Quart. Jour. Med., 1911, iv, 267.
  11. Birk: Mü Wchnschr., 1912, lix, 1429.
  12. Hutchinson: Clin. Jour., 1911, xxxviii, 209.
  13. Thiemich: Jahrb. f. Kinderh., 1910, lxxii, 243.
  14. Müller,A.: Ztschr., f. Urol., 1912, Suppl.
  15. Friedenwald: Arch. Pediat., 1910, xxvii, 801.
  16. Walker, J. W. T.: Practitioner, 1911, lxxxvi, 655.
  17. Leutscher: Bull. Johns Hopkins Hosp., 1911, xxii, 361.
  18. Rolleston: Practitioner, 1910, lxxxiv, 439.
  19. Stewart: Univ. of Penn. Med. Bull., 1910, xxiii, 233.
  20. Collica: New York Med. Jour.,1911, xciv, 376.
  21. Franke: Mitteil. a. d. grenzgeb. d. Med. u. Chir., 1911, xxii, 623 and 1911, xlviii, 1973.
  22. Clarke, W. B.: Clin. Jour., June 28 and July 5, 1911.
  23. Chambard: Ann. d. mÉd. des org. G. U. 1911, xxix, 865.
  24. Pardoe: Brit. Med. Jour., 1910, ii, 1129. [Full Text]
  25. Dick: Brit. Med. Jour., 1910, ii, 1134. [Full Text]
  26. Betz, Meyer: Deutsch. Arch. f. klin. Med., 1912, cv, Nov. 5-6.
  27. Briscoe: Lancet, London, 1909, ii, 1269.
  28. Casper and Citron: Ztschr. f. Urol., 1911, v, 241.
  29. Sisson: Unpublished communication.
  30. Geraghty: Tr. Congress Am. Phys. and Surg., 1910, viii, 271.
  31. O'Neil, R. F.: Am. Jour. Urol., 1911, vii, 209.
  32. Williams, R. S., Murray, H. L., Wallace, A. J.: Jour. Obst. and Gynecol. Brit. Empire, 1912, xxii, 65.
  33. Williams, Craigin and Newall: Tr. Congress Am. Phys. and Surg., 1910, viii, 148.
  34. Cabot, H.: Am. Jour. Urol., 1911, vii, 131.
  35. Pringle, S.: Practitioner, 1911, lxxxvii, 35.
  36. Lyman, C. B.: Northwest Med., 1911, iii, 31.
  37. Koll: Amer. Jour. Urol., 1912, viii, 287.


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