Infantile beriberi

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Part of Acta Medica Philippina

Title: Infantile beriberi
Language: English
Year: 1947
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Fulltext: INFANTILE BERIBERI IN THE PHILIPPINES JosE ALBERT, M.D.* and MOISES B. ABAD, M.D. Department of Pediatrirs, College of Medicine, University of the Philippines, and the Philippine General Hospital There are problems of beriberi in general and of infantile beriberi in particular which are still unclear, and probably will remain so for a long time, since "medicine is not, and never will be, an exact science." In this report, we have restated some of the most important of these problems, in the hope that by considering them against the. background of data gathered from 968 cases of infantile beriberi seen in the Pediatrics Ward of the Philippine General Hospital from 1914-1946, possible solutions or fresh approaches might become apparent. Etiology.-Although beriberi was known to the Chinese as early as 2600 :a. c. and to the Romans as early as 24 B. c.(2), its etiology is not settled. The prevailing opinion i~at it is a. nutritional deficiency disease. Until recently we accepted this opinion and believed that Vitamin Bt was the deficient factor. However, recent studies have forced us to modify this opinion. a. Race.-In 1931, Albert reported a series of 500 cases of infantile. beriberi in which he pointed out that the condition was not seen among Caucasians or among the offspring of CaucasianMalayan parents. The explanation given was the difference in diet and social scale; but low-income families, where the diet is obviously inadequate, ar~ found in all groups-Caucasian, mixed, and Malayan. b. Age.-Infantile beriberi, as the term implies, occurs almost exclusively during the first year of life. As can be seen in Table 3 the most dangerous period is 1-4 months. During this time, the disease is most frequent as well as more severe. Guerrero and Quintos(9) stated that the greater number belong to the group between one and three months old. Beyond the age of one year we do not see the disease. Why does beriberi affect only infants and adults and spare young children? Obviously, a thiamin-deficient diet cannot. be the only answer. * Doctor Albert died on August 13, 19+6. 7 8 Acta Medica Philippina c. Monthly Variations.-Humidity, rainfall, temperature, atmospheric pressure probably exert some influence, for although infantile beriberi is found throughout the year, the incidence is significantly lower during the months of May and June and highest during November, December and January (Table 2). d. Yearly Variations.-In May, 1928, Albert and Ocampo(3) published a paper wherein they voiced the opinion that "infantile beriberi was disappearing at least in Manila and its environs." They attributed this success to the combined efforts of the Government, through its health agencies, private physicians, nurses, etc., who have popularized the use of tikitiki extract, and to the education of the masses in proper infant feeding. This situation did not last long. For the very next year, 1929, the incidence of the disease began to rise again and remained high for the next eleven years. Then from 1941 to the middle of 1946, another period of decline set in. In other words, the cycle from decline to decline seems to be 12-13 years. The first period of decline, lasting for three years, began in 1926; the next period of decline started in 1941 and continued up to the middle of 1946. From the other services in our Hospital (Medical and Obstetrical) and from other clinics in Manila, the same decline was noted. This period coincided with the Japanese occupation when food shortages became acute and death from starvation was an everyday affair. Generalized malnutrition, "hunger edema," xeropthalmia, keratomals.cia, hyperkeratosis, and cancrum oris were frequently /f!een in our Out-Patient Clinics as well as in the wards. And yet infantile beriberi practically disappeared during this period. e. Associated Diseases.-Infection plays an imrortant though undetermined role in the etiology as well as the course and prognosis of infantile beriberi. Guerrero and Quintos(9) classified infantile beriberi into pure and mixed, the latter being associated with gastroenteritis, bronchitis or convulsions. In our cases, more than half were seen with some form of infection, either frank or subclinical, since fever, cough, or diarrhea was frequently present. The most commonly associated diseases were bronchopneumonia, bronchitis, and enteritis. These were often responsible for the flaring up of symptoms, and were often the cause of death in the cardialgic forms of beriberi. Albert, Abad: Infantile Beriberi 9 f. Feeding.-All observers recognize breast-feeding as the condition "sine qua non" for the development of infantile beriberi. However, from time to time, cases occurring in bottle-fed infants are reported. Chapman(12) described 8 such cases in 1927. Since 1931, I have seen twelve cases among bottle-fed and forty-five among mixed-fed babies. In the last group, the information was usually obtained that the infants were nursed by their mothers for a period varying from one week to two months from birth. When the symptoms first became apparent, they were being artificially fed, and had been so for some time. In view of all the above considerations, the conclusion seems inescapable that infantile beriberi is not simply a vitamin deficiency disease, and that other factors, besides lack of thiamin, are involved. Of course the most important factor seems to be faulty nutritional· habits. The nursing mother of the stricken infant, . when carefully. questioned, usually revealed that she had been subsisting on a monotonous diet consisting of excessive quantities of polished rice, some fish, and little or no meats and vegetables. Acco.g to McCarri~ son(13) such a diet has at least four faults, namely, poverty in pro~ tein, excess of starch, deficiency of calcium, sodium and chloride, and lack of Vitamin A and B. Just exactly what role the secondary factors, enumerated above, play in bringing about the: full-blown clinical picture of infantile beriberi cannot be determined at this time. CLASSIFICATION Various ways of classifying infantile beriberi have been proposed, based mostly on symptomatology. After studying our 968 cases, we believe that they can be divided into five groups. L Pure Cardialgic, Fulminant or Pernicious Type. The onset is characteristically explosive. Vomiting after sucking may be the only prodromal symptom. The most important features in the clinical picture are as follows: a. The baby is plump and apparently well nourished. b. The baby's cry is a peculiar loud, piercing. and persistent scream repeated in paroxysms, apparently denoting severe suffering. This gradually gives way to a moaning or whining sound, as the child becomes exhausted. c. The face is markedly pale, with a cyanotic tinge around the mouth. 10 Acta Medica Philippina d. The patient's body is stretched out, it may become stiff, and towards the end, convulsions may be noted. e. The atdomen shows some rigidity, simulating rlatui.ent cciic. f. Respiration is labored. In the agonal stage, the baby gasps for breath, the eyes staring upward. g. Auscultation of the heart reveals accentuation of the see:ond pulmonic. h. Roentgenography shows an enlarged heart. i. Therapeutic test with thiamin elicits a dramatic cnauge in tbe clinical picture within one-half to six hours. On the other :i:1and, cardio-tonics as caffeine, digitalis, and strophantin are ineffective. The clinical picture derived from the above manifestm:io:ns is almost characteristic. A baby around three months old, apparently in good health, nursed entirely by its mother, is abruP,tly seizecl with an attack of screaming. As he utters his loud piercing cry, his body stretches, the abdomen becomes hard, the pulse thready, the respiration labored, his face either deathly white or cym10tic, and an expression of profound terror or suffering grips his entice o.eiag. This state may last. anywhere from one half to one hour. It cii&appears spontaneously, only to recur with increasing severi.ty and • frequency until death supervenes, or the specific treatment is promptly administered. The Aphonic Type Unlike the first group, this is characterized by an insici~ous onset and a long duration. It is much less serious than the carciialgic form. The outstanding feature is the dysphonia in some cases a.1.1d complete aphonia in others. These cases usually begin with a siight fever and cough, or choking, and for this reason, are often mistaken for upper respiratory tract infection. As in the first, pallor of the face, with cyanosis around the mouth, is also seen. Restlessness, paroxysmal polypnea, oliguria and edema: are often noted. The aphonia may be severe. We saw a case iri which restoration of the voice did not come until after some months, although all other symptoms had long since disappeared. When well developed, it also gives an unforgettable picture. As irt the cardialgic type, the baby seems to be crying, but because of the loss oi voice, no soU1id conies from him, and only his grimaces and. twitching of his face offer evidence of the sufferings he is undergoing. Albert, Abad: Infantile Beriberi 11 The laryngological examination is revealing.. Alcantara . a_'ld Ocampo(IS) reported their findings in 37 cases in 1939: "The five infants with acute cardialgic beriberi in whom impairment of voice was slight showed only congestion of the vocal cords, motility being normal. All the rest had impairment of motion. The right vocal cord was paretic or could not move to the median line in 4 cases, stayed immobile in the rniddle in 9 cases and ·assumed a cadE1.veric position in 3 cases. The left vocal cord was paretic in 5, completely immobile in the median line in 9 and cadaveric in 1 case. '!'he vocal cords were bilaterally affected in 3 cases. In some cases, the paretic vocal cord appeared at a lower level than normal." This group showed the poorest response to thiamin: Tho Pseudomeningitic Type . This type, first described by Albert in 1917, presents a distinct pkture from the first two types. It is also less common, and is more often observed in older infants, between 6f1iib.d 12 months of ase. The typical picture is that of a well-nourished baby, breast-fed, who gradually becomes peaceful and quiet, as if he has forgotten how to cry or smile. He wears a languid and indifferent look, hl.s eyelids are but half open. Sometimes, in addition to the ptosis of the u9p"'lr !.ids, there is strabismus or nystagmus, suggesting ence·phalitis or tuberculous meningtis. There is, however, generally no nuchal rigidity. There may be spasmodic contraction of the facial musdes or choreic movements of the arms and hands. Sometimes there may be convulsions so severe as to require lumbar puncture. Vomiting and moderate constipation are noted. The temperature may rise to 3s.oc. In 1934-1935, when we had an unusual number of these cases, the ,iunior author made an observation which we thought might be useful in the differential diagnosis. We noticed that these cases of pseudom,.epingitic beriberi, in spite of their lethargic appearance, r-;sponded normally to certain stimuli. When a toy or any object was presented to one of these patients, in spite of his apparent stupor, he would reach out an unsteady arm to get the object offered to him. A similar stimulus given to patients with encephalitis or men. ingitis brought no response. Often these. cases are erroneously diagnosed as meningitis and progress to a fatal termination. Such errors are all the more tragic 12 Acta Medica Philippina because of the fact that thEse casEs rEspond promptly to large doses of thiamin. The Mixed Type In this group are included those patients who show a combination of symptoms of the first three groups. Thus we have the (a) cardialgic-aphonic type (b) the cardialgic-pseudomeningitic, and ( c) the aphonic-pseudomeningitic. The cases that fall into any of the four groups described above are not hard to diagnose. There are, however, certain cases that prcs<mt only a part of the symptom complex and thereby become major diagnostic problems. In some, the gastro-intestinal symptoms are most prominent, in others cyanosis. The diagnosis is often made by inference and the response to specific therapy. This group may probably be labelled the attenuated form or the "formes frustes." THE PROBLEM OF THERAPY Chamberlain and Vedder reported in 1912(18) that an extract of rice polishings ( tiki-tiki) was effective in beriberi. Since then confirmation has come from all parts of the world. The reduction of infant mortality in the Philippines from 65'/c to about 20% is considered to have been largely due to the extensive use of tiki-tiki extract. Its prophylactic and curative effects can no longer . be doubted. In spite of this, however, we find that only ;:ibout 3 l % .. of our cases were cured; the rest died or were dischafged partly improved. We offer the following tentative explanation: 1. Those recovered were pure uncomplicated cases of the cardialgic and pseudomeningitic types who were brought in for early. treatment. 2. Those that died were brought in too late or had some com..: plicating acute infection. 3. Those that showed partial improvement only, without complete recovery, were mostly cases of the aphonic type. · Although the symptoms of restlessness, pallor, edema, oliguria, etc. disappeared rapidly with the specific treatment, aphonia or dysphonia persisted· for months. In this case, thiamin apparently had no effect on the paretic vocal cords. These questions therefore come up: Is aphonic infantile beriberi true beriberi or something else? If it were true beriberi, why is 6 0 0 • L I , t £ '/ ~ ' r ~ ., c I ~ ') ' b I I ·-~', --- . ... -s ~ s ~ ;:> /(J ·o IV ~ ~ '() ~ ~ ~ C'..f. ....... ~-...... '.\ -~ ~:. .Jli( __ ..,} -o..... , ..... Q I ' - ---~ / -- I< 0 1qq.r 1ql/L1 1q113 1q4Z 1941 /"IL/ 0 I- - - _"b - L> 1939 /t/;Jf 1937 lf36 ;q3s p.r-.... - p.--... ,_ QI' . .... o,.._ - r----· ~-...o .... " . , .. .. c .. )> ii '{- . 'r-..... - ... n }} ,· lo'/" i>"' 1 --~ ~,-"}>' ) h..,\ / _..._"> .;! ~7 __ ..... -- ~• -~ - /'· = 1-0 "'l> ~ ;;;,O!:lfUJ")J~d PJY/. 1933 1q3z /Cj31 /tfJO IC/JJJ 192.( 1qz7 1q26 /qi/) 1124 19J.3 ./ l/J.?. qz1 I I qzo ql'l 91~ I I I f 111 ~?16 I I q15" q14 (.) ~ "" /"- 160 150 140 130 120 /10 100 90 ff O Vl ~ 70 \t) ll' ~ () °"> 50 ~40 Q 30 <! zo /0 0 - \ \ \ \ \ \.___ "' Jqn. Fe/,. Ma,.. .. ' '/ I / .; / - ·/ __,/ "'.. / ......... ./ r--... " v "'-tr Gpr. May Ju11. Jq/. Ou1· Sep/. Ocf. Nov. /Jee. Monfhly Disfr/buf/011 of I;;jBen1er1 Albert, Abad: Infantile Beriberi 13' thiamin ineffective? Does it represent one of the irreversible stages of polyneuritis? Remembering that most of the symptoms associated with the aphonia were quickly and favorably influenced by thiamin, one is inclined to consider that this type is a true beriberi. Doubt about thiamin being an "antineuritic vitamin" has ·been expressed in various quarters. Thus it is well known that in adult beriberi _it is ineffective, except for the relief of cardio-vascular manifestations. Aring and Spies(20) and Ming(Zl) believe that the initial prompt improvement with thiamin in cases of nutritional deficirncy is humoral in nature. Peters ( 22) thinks that it acts as a catalyst in the carbohydrate metabolism of the nerve cell and of the heart muscle, so that its action in beriberi subjects is concerned with the reestablishment of the normal metabolism of the carbohydrate in the tissue. Walse(23) accordingly says: "To speak of Vitamin B1 as 'antineuritic' is wholly erroneous except in relation to cases (human and avian) receiving a high carbohydrate diet.", Meiklejohn(24) makes the following conclusions: 1. Thiamin is capable of curing a specific metabolic disturbance in the_ nervous . system in animals. This disturbance has been inco.rrectly referred to as "polyneuritis" by many authors. 2. There is yet no clear experimental evidence showing that true am;i.tomic polyneuritis in animals is curable by thiamin. Thiamin deficiency in animals disturbs not only the normal metabolism of the nervous tissue, but also, and in a similar manner, the metabolism of the kidney, heart and probably other organi;. It so happens that the metacolic disturbance of the nervous tissue manifests itself externally in a dramatic manner, while a similar disorder proceeding in the kidney and elsewhere produces no such obvious effects. This has given rise to the erroneous belief that thiamin has a specific effect on the nervous tissue. It is. probably safe to say that thiamin is necessary for the normal metabolism of almost all tissues. . It would seem that so far as the evidence from laboratory experiments is concerned, there is really no gre!it justi-. fication for referring to thiamin as the '(antineuritic vitamin." . SUMMARY L A study based on 968 cases of infantile beriberi seen in the Pediatrics wards of the Philippine General Hospital is presented. 2. The disease seems to have definite phases of intensity and decline, following a cycle of 12-13 years. Acta Medica Philippina 3~ Seasonal variations, age, sex, etc. are de£iPite S")cnndary fact"!'S in the etiology. ~- Th~ disease, as usually observed in our wards, usu?-11";!' c-::curs in ?"!"lociation with upper respiratory tract or gastrc-i:ntrt:c.-.n1 infoctisn"~ 5, Classification of the disease, based on sympto:!'.12t0logy, is pro."l~nt~d. c. Evidence that the condition is not due solely to vitf'.:r::dn B1 d'!fidency is given. REFERE:'\CES ( 1) Fx.•SE!I., H. and STAKTm:, A. T.: Collected Papers on Ee1·iberi. Lo!'.don. John Bale, Sons & Daniel"on. Ltd. (1924-). (::n J\um·:.T, JosE ~nd OCAMPO, A. :\!.: ls Infantile Beriberi Dis~9..,earing? Jo·H. P. I. Med. Assoc., Vol. 8, No. 5, 221 2Z+, May, ln8. ( ~) Dr. MANAS, Puericulture Center of ]\If aka ti, Rizal, and Dr. A. REG.'>.LA, Oro~uieta Maternity and Children Hoc;pital, Manilr.: P~rso'."d ~ommu D~,cu.tio-ns. (5) OcM!PO, A. N., and HERRERA, !\. A.: Avitaminosis A V"'ith SpedF] Peference to C1'taneous Manifestatiom. Paper read at the Conference o~ t.1~dicaJ Sciences, Dec. 20, 21, 22, 19+3, Manila. (5) GA!', TOMAS M., MATIAS, M. Y. CRUZ, A. H., and SAN ]UH<, .Tr": \Y~.rtime Hypovitamin~sis A: A Preliminary Report. Paper reao ~t ·th.e Co<".f~r ence 0!1 Medical Sciences, !Vfanila, Dec. 20, 21, 22, 194~. (7) ALBE":T, ]osE and PECACHE, L. V.: lncidrnce of Cancrum Oris ei~e tl-e Outbreak of the Greater East Asia \Var. lbid. {") G'JEr.RERO, M. and Qurnrns, ]. : El Beriberi rn los Ninos de J;>2c1'c. M:rnila (i910). (12) CHAPMAN, LELANDS S.: Infantile Beriberi in Panama. A Prelimiroary Report. Proc. Med. Ass. Isthmian Canal Zone 14 (1921-1~25), 37_1,g, Abstract in Trop. Dis. Bull. 25 (] une, 1928) 4-32. (1.3 ). McCARRisON, R.: The Relaticnship of Diet to the Physic2.1 Effici~ncy of Indian ~aces, The Practitioner, Jan., 1925. ( 15) .t\r,cANTARA, V. C. and DE OcAMPO, G.: The Larynx in Inf :rntile Beriberi. A~chiv. Otolaryngo!ogy, Vol. 30, 389-399, Sept., 1939. (16) ALBERT, JoSES La Forma f'seudomen:ngiticJ. del Beriberi Infartil. Rev. Fil. de Med. y Farm. Vol. XI, 1': o. 1, Jan., 1920, p. 11. {!8) CHAMBERLAIN, W. P. and Vrnorn, E. B.: The Cure of Infant\1~ Eerib~ri by the Administration to the Infant of an Extr<:ct of Rice Polishing, and t:1e Bearing Therecf on the Etiology cf Beriberi. Bull. Ma!li!a Med. Soc., 6 No. 2 (1912) 26-29. (19) Liga Nacional para la Proteccion de la Primera Infancia. (Fift'i Report to the Legislature. Rev. Fil. de Med. y arm., 10 Mayo, 19B). (20) ARING, C. ET AL.: Some Clinical N eurologic Aspects of Vitamin B .Deficiencies. J.A.M.A., 113 No. 2+: 2105-2109, Dec. 9, 1939. Albert, Abad: Infantile Beriberi 15 (21) Mi:.;Z, BRUNO: Le role de la vitamin B1 dans la regulation humoraie du System Nerveux. Presse Med., +6: 1406-1407, Sept. 21, 1938. (22) F.<TE:i:.s, R. A.: Lance), 1: 1161-1165, 1936. ( 23) ·;,v ,:.LSii2, F. M.R.: ,C.etio!ogy of Polyneuriti,. Lancet, 1: 3 3-3 5, j an. 11, H'rl. (2-r) 1'ili"LEJOIIN, A. P.: Is Thiamin the Antineuritic Vitamin? N. Eng. J. 11.ied., 2'.B: Z65-273, Ang. 22, 19+0. (25) CLENilE>1rnG, L.: A Letter to the Editor, J.A.M.A., 117: 1036, Sept 20, 19+1. 16 Acta Medica Philippina TABLE I.-Percerdage of infantile Beriberi :\o. fj~· CASES OF PERCENTAGE DIYEAR INFANTILE BERIBERI TOTAL ADMISSION INFANTILE BERIBERI - - - - - - - -------- -~·------1914 51 547 9.32 1915 45 577 7.79 1911} 52 591 8.79 1917 51 866 5.89 1918 40 1127 3.55 1919 24 792 3.03 1920 37 1091 3.39 1922 39 1171 3.33 1921 37 103(1 3.59 1923 +6 1276 3.61 1924 19 1369 1.39 1925 18 1383 1.30 1926 9 1408 0.64 1927 6 1316 0.46 1928 6 1344 0.45 1929 19 1573 1.15 1930 15 1712 0.88 1931 21 1853 1.13 1932 3+ 1955 1.74 1933 62 2092 3.01 1934 71 2318 3.07 1935 79 2767 2.85 1936 36 2377 1.51 1937 +2 2306 1.82 1938 19 1953 0.97 1939 25 2008 1.24 1940 33 2390 1.3~ 1941 16 2157 0 70 1942 7 928 0.75 1943 0 916 0 1944 0 907 0 From July 16Dec. 31 1945 () 916 0 1946 9 264R 0.34 YEAR 1914 1915 1916 1917 1918 1919 1920 1921 1922 1923 1924 1925 1926 1927 1928 1929 1930 1931 1932 1933 1934 1935 1936 1937 1938 1939 1940 1941 1942 1943 1944 194S 1946 Total }AN. 5 4 8 4 5 7 3 14 3 7 3 I 2 3 1 1 s 8 5 27 9 8 4 2 8 3 150 FEB. 4 3 6 2 7 1 1 1 2 i 2 4 1 1 2 2 9 8 11 2 7 4 1 3 1 1 86 MAR. 3 1 3 3 6 1 6 4 10 2 3 2 I 3 10 5 7 4 3 1 2 2 84 TABLE II.-M onthly Distribution of Cases APR. 1 3 2 11 6 1 4 3 2 2 2 3 I ! I I I I . I I I: I s I 1 · I 6 I 2 I 3 2 2 62 MAY 1 6 2 2 1 2 2 2 3 3 2 1 4 4 4 1 1 2 1 1 49 JUNE 2 2 3 3 2 1 1 1 0 1 1 2 1 3 3 2 1 3 1 37 jULY 2 1 3 3 1 1 3 4 2 1 2 3 3 l 3 6 I I I I I ~ I ; ( 1 ~ ~ 1 52 AUG. 2 1 3 2 1 2 1 3 5· 4 1 2 3 1 4 5 3 2 2 l 2 1 53 SEPT. 6 4 1 3 2 1 4 1 5 2 1 2 1 1 3 2 5 3 3 4 4 4 4 l 3 4 74 OcT. 6 5 4 7 1 2 4 2 2 3 2 1 1 3 2 l 4 1 8 6 3 1 2 3 3 2 1 81 Nov. 1~ l 4 I ! I ~ I 3 I 3 I I I I I 1 I 6 I 6 I ; I 1 I 1 I I 1 I 4 I 1 I 103 I I \ DEC. I s I 9 9 7 8 5 13 5 6 5 1 1 1 1 1 4 1 6 5 3 22 5 1 2 2 1 4 1 137 I TOTAL1 51 45 52 I 51 40 24 37 . 39 37 46 19 18 9 6 6 19 15 21 34 62 71 79 36 42 19 25 33 16 7 0 0 0 9 968 ). tr ~ ~ ..... ). O' Ill ~ i ..... :::.; CD bs (11 "t 5' ~ .... ~ l8 Acta Medica Philippina TABLE III.-Incidence of Infantile Beriberi by Age Group YEAR 0-1 WK. i 2-+ WK:. i 1-3 Mos. 1 +-6 Mos. i 7-12 Mos.! TOTAL 1914 9 3+ 4 3 51 1915 9 22 8 5 +s 1916 7 33 9 3 52 1917 4 33 8 6 51 1918 4 19 8 9 40 1919 7 7 3 7 24 1920 5 20 7 5 37 1921 5 17 9 8 39 1922 7 18 6 6 37 1923 2 8 26 9 1 46 1924 2 12 2 3 19 1925 3 13 18 1926 2 4 9 1927 4 2 6 1928 3 1 2 6 1929 10 6 3 19 1930 4 3 8 15 1931 10 2 9 21 1932 18 10 6 34 1933 34 15 13 62 1934 29 20 22 71 1935 31 23 25 79 1936 18 15 3 36 1937 20 14. 7 42 1938 10 6 3 19 1939 12 5 8 25 1940 18 12 3 33 1941 9 4 3 16 1942 2 1 4 7 1943 0 1944 0 1945 0 1946 6 9 Total 4 71 494 220 179 }-1 Percentage 0.41 7.33 51.03 22.72 18.80 TABLE IV 1931 I 1932 I 1933 11.934 I 1935 I 1936 I 1937 I 193$ I 1939 I 1940 , .1941 I 1942 I 1943 I 1944 I 1945 \ 1946 I TOTAL A. No. of Cases . . . . . . . . . 21 34 I 62 71 79 · 36. 42 : 19 I . 25 I 33 16 B. Types : · I I I 1. Cardialgic . . . . . . . . . 13 20 t 26 43 · 36 . -16 16 6 I 5 \ • 12: 4 2. Aphonic .. .. .. .. . .. . 3 7 \ 26 · 6 11 · 9 7 2 \ 4 I 9 6 3. Pseudomeningitic . .. 5 6 I 5 7 · 11 3 4 1. I 7 I · 5 1 4. Mixed: I I. I a. Card.-Aphon. . . . . I 1 6 10 7 · 14 9. I 8 I 7 5 b. Card.-Pseudo . . . . I 1 · 2 I I c. Aphon.-Pseudo. . . \ 2 \ • I S. Frustrated: I I ) · (attenuated) · 1 I I a. Gastro-intes. . . . . I 3 1 I I b. Cyanotic ..... .'. . . 1 I 4 3 8 1 1 1 I 1 I C. Sex: I 41 ·48 20 \ \ 1. Male . . . . . . . . . . . . . . 11 t9 ·I 35 30 31 16 30 10 I · 12 I 18 9 2. Female .. .. . .. .. . .. io 15 I 27 · 12 9 I 13 [ 15 7 D. Feeding: I \ \ 1. Breast alone . . . . . . . 19 27 \ 61 55 71 30. 39 18 I 21 I 31 12 2. Bottle fed . . . . . . . . . 2 I 1 · 1 2 1 · 1 I I 1 1 ·· 3. Mixed fed .. .. . .. .. 2 5 I 1 15 . 7 4 2 I 4 I 1 3 E. Outcome: I I I 1. Recovered . . . . . . . . . 8 10 . \ 16 21 23 12 14 6 I 9I I 10· 5 2. Im~roved .. .. .. . . .. 3 7 ·I 28 16, 23. 10: 19 10 .1 11,.,1·20 9. 3. Ummproved . . . . . . . . 3 1 I · \·· 2. 4.Dit>ri ...... , ....... 10 11 I 18 ~4 30 13 9 3 I 5. I 1 2 7 :i 2 2 1 6 1 4 2 1 4 3 0 0 0 0 I . I ::. I I 0 0 9 454 4 203 2 94 55 3 72 3 3 4 20 5 264 4 190 9 397 12 45 7 141 1 161 6 1 146 :i:.. l :i:.. O< Ill ~ 5" Q;::3 .... ==:.: (1) to ~ ~ ... .... IO