A STUDY 
OF 
CERTAIN PREVENTABLE DISEASES, 
THE CAUSES OF DEATH 
AND 
METHODS OF PREVENTION 
Dedicated to the Local Health Officers 
of Texas in appreciation of their un- 
selfish service to humanity. 
Geo. W. Cox, M.D., 
State Health Officer 
TEXAS. STATE DEPARTMENT OF HEALTH 
AUSTIN% TEXAS INDEX 
Page 
PNEUMONIA 3 
WHOOPING COUGH 6 
INFLUENZA 12 
SCARLET FEVER 15 
MEASLES 23 
TUBERCULOSIS 29 
DIPHTHERIA 35 
POLIOMYELITIS 1+0 
TYPHOID 1+7 
DYSENTERY 57 
MALARIA 65 
1/CANCER 82 Foreword 
This bulletin is published with the hope that it will prove to be of 
benefit as a ready reference concerning the handling of the diseases which are 
of major concern to the health officer and other public health workers. 
So far as possible, controversial points have been avoided in the 
preparation of this bulletin, and it is by no means intended to replace 
standard text books and such information as may be gathered from the current 
literature. It is suggested that the book might be most profitably used 
in connection with U. S. Public Health Service Reprint Number 1697, titled 
"The Control of Communicable Diseases". This periodical may be purchased 
from the United States Government Printing Office in Washington, D. C., at 
a price of five cents. In ordering these bulletins, address the Superin- 
tendent of Documents. It is suggested that the health officer might profit- 
ably place a copy of this latter bulletin in the hands of each practitioner 
in his community. 
Every physician in the community should be familiar with the diseases 
that are reportable and with the provisions of the law concerning the quaran- 
tine of these diseases. In communities where a full-time health officer is 
available, the practitioner can reasonably expect the following upon report 
of a contagious disease: (l) that the premises will be visited by the 
health officer or his representative and that legal quarantine or isolation 
will be established and that the disease will be reported to the State 
health authority as required by law; (2) that in those conditions where 
epidemiological study is often fruitful of results, a case study of the 
origins of the disease will be made; (5) that instructions will be given the 
family as to the methods of disinfection and sterilization which are most 
practicable, and that suitable bacteriological procedures will be Instituted 
to determine the carrier's state before releasing him from quarantine; 
that the health officer and his representatives will in no way interfere 
“with the treatment of the patient or patients, since this does not fall 
within the field of public health; (5) that all contacts to the infection 
will be either Immunized by the health officer or urged to visit their 
private physician for immunization if the disease be one in which immuniza- 
tion is effective; (6) that the health officer will be responsible for all 
legal measures that are necessary to prevent quarantine violation. 
The foregoing activities relate chiefly to the duties of a full-time 
health officer. In communities having part-time health officers, any or all 
of these activities may be performed; however, many of our part-time health 
officers are paid little or nothing for their services and cannot afford to 
leave their practices to do the work normally carried on by the full-time 
health officer. In such communities, practitioners should report to the 
part-time health officer, but in many instances they will be delegated 
to establish quarantine and supervise disinfection, etc. It is imprac- 
ticable for private practitioners to do a great deal in the way of 
epidemiological study, since such study usually leads to the homes of individuals who comprise a portion of another private physician's practice. 
To attempt to arrive at sources of infection often results in friction 
between the practitioners. 
While the epidemiology must usually he neglected in such cases, the 
bacteriological studies to determine presence or absence of the carrier's 
state can be, and by all means should be carried on. Since it is more to 
the public interest than to the individual's interest that these studies 
be made, they will be done in the State laboratories regardless of the 
economic situation of the patient. If carriers are found, these, too, 
should be reported to the local part-time health officer just as cases 
are reported. 
A limited amount of epidemiological service is available from the State 
Health Department to communities not served by full-time health officers. 
In any situation which seems to warrant an epidemiological study, a request 
should be made for such service to the State Health Officer. However, on 
arrival of the State Epidemiologist in your community, it is necessary that 
he have some sort of records with which to begin his work. He must know 
who the patients are, where they live, their ages and occupations, and 
similar data. These data are easily collected by local practitioners on the 
cases in their practice, but it is extremely difficult for the visiting 
epidemiologist, a stranger to the community, to accumulate these data. 
Until they are accumulated, he cannot do any effective work. 
It must be remembered that every practitioner who encounters reportable 
contagious disease is legally responsible for the spread of the disease to 
others if he does not report it to the proper local health authority. 
Courts have repeatedly awarded damages to individuals who have contracted 
a disease from an unreported case. Their cause of action is against the phy- 
sician treating the case, and his only possible defense is that he had failed 
to make the diagnosis. Naturally, such an admission does a physician little 
good, even though he may escape paying damages on the basis of this plea. 
Once a case is reported, however, the acting physician is exonerated from 
all blame in the event of subsequent spread of such infection even though 
the local health officer takes no action to control the disease. YEARS OF AGE 
DEATHS FROM PNEUMONIA IN TEXAS 
IN 1938 
BY AGE 1 
TOTAL DEATHS-4149 
KEY -EACH MAJOR GRID 
REPRESENTS 60 DEATHS PNEUMONIA 
Pneumococcus pneumonia is a communicable disease. This fact 1s well 
demonstrated by the occurrence of multiple cases In families, cross-infections 
in hospital wards, and the large number of epidemics that have been observed 
annually in New York State and elsewhere. The patient with pneumonia should 
be kept in a room by himself, and all visits by individuals other than the 
attendant and physician should be kept at a minimum. Those constantly 
attending the patient should wear a gown or large apron over their clothes, 
and this should be removed on leaving the sick room, following which the 
hands should be thoroughly washed with soap and hot water. All grossly con- 
taminated articles should be cleaned and sterilized as completely as the 
nature of the article permits. Sputum should be collected in clean cloth 
or paper mouth wipes or, if a sputum cup is preferred, in an inflammable 
container so that it may be burned. Provision for isolation, however, 
should not be so elaborate as to interfere with the proper nursing care of 
the patient. 
Etiology and Prevention 
A. Causative microorganisms. 
1. Pneumococcus. Responsible for 95 per cent of the so-called 
lohar pneumonias and approximately 50 per cent of the so-called 
hroncho-pneumonias. Pneumococci classified into 52 specific 
strains called types, designated hy Roman numerals. 
(a) Types I, II, and V especially prone to cause adult lobar 
pneumonia, 
(b) Types XIV, VI, XIX, and I most commonly encountered, in 
order given, in pneumonias of infants and children. 
(c) Types III, VII, and VIII frequently found in cases of 
both lobar and bronchopneumonia. 
2. Other microorganisms such as streptococcus hemolyticus, 
staphylococcus, Frledlander’s bacillus, and influenza bacillus 
are responsible for the most acute pneumonias not pneumococcal 
in origin. In some cases of pneumonia, even after careful 
study, the etiological agent cannot be determined. The possibi- 
lity that such cases are caused by filtrable viruses has been 
considered but not proved. 
5. Acute pneumonic conditions may accompany other infectious 
diseases as secondary manifestations. 
B. Communicability 
The occurrence of localized epidemics, of multiple cases in 
families, and of cross-infection in hospital wards is sufficient 
evidence to justify the conclusion that many types of pneumococcus pneumonia are communicable diseases. Contacts of 
a case frequently are found to be carriers of the same type of 
pneumococcus as that found in the patient. 
C. Source of infection. 
1. Respiratory secretions of Infected individuals, convalescents, 
and health carriers. 
2, Probable paths of transmission. 
(a) Direct: by droplet infection. 
(b) Indirect: through contaminated articles or dust in con 
taminated surroundings. 
D. Predisposing factors 
It is generally felt that infection resulting in pneumonia is 
somewhat dependent on the existence of certain predisposing 
conditions which act by lowering the resistance of the host and 
increasing his susceptibility to that particular type of infec- 
tion. Specifically, these conditions are thought to be such 
infections as the common cold, grip, Influenza, measles, and 
whooping cough. Also, the post-operative period, chronic 
debility, abnormal fatigue, over-exposure, chilling, and alco- 
holism generally are considered important in this respect. 
E. Preventive measures. 
It should be borne in mind that the following "preventive measures 
are founded on what might be called ’’common sense rules” rather 
than on established scientific fact. Since the true chain of 
events leading to pneumonia is not known, the elaboration of 
scientific methods of prevention is, of course, impossible. 
1. Protection of individuals with lowered resistance from unneces 
sary exposure to pneumonia or possible carriers. 
2. Avoidance of predisposing conditions. 
3. Maintenance of bodily resistance through adequate personal 
hygiene, which includes adequate rest, nutrition, exercise, 
and warmth. DEATHS FROM WHOOPING COUGH IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-315 
KEY-EACH MAJOR GRID 
REPRESENTS 20 DEATHS WHOOPING COUGH 
(PERTUSSIS) 
Whooping cough is a specific infectious disease of the respiratory- 
tract caused by a bacillus, Hemophilus pertussis, and characterized by a 
preliminary catarrhal stage followed by a spasmodic stage with a whooping 
type of cough. 
Historical - First described by Baillou following an outbreak in 
Paris in 1578; studied by Willis and Sydenham in England I658-I67O; 
appeared in Germany I72U; America 1732; New Zealand l8Vf; Australia, 
1890. 
Etiology - Hemophilus pertussis discovered by Bordet and Gengou in 
1906 - a small, gram negative, non-motile rod requiring hemoglobin for 
culture. The organism grows profusely on the cilia of the epithelial 
cells lining the trachea and bronchi, causing irritation and secretion 
of mucus. Can be cultivated from cases best by the cough-plate method, 
using petrl plates containing potato-glycerine-agar with human blood. 
It has been thought by some that a virus might be associated with H. per- 
tussis in the etiology, but this has been excluded by the production of 
the disease in humans and anthropoid apes, .using pure cultures of the 
organism, and by failure to produce the disease with filtrates from such 
cultures. 
Geographical Distribution - Endemic throughout the world except in 
a few places like the Faroe Islands in the North Sea, where it appears 
in epidemics at Intervals of four to six years. It is as prevalent in 
warm countries as in colder climates, but causes less fatuities in warm 
climates because of the lower incidence of complications. 
Seasonal Incidence - In most countries the disease is constantly 
present throughout the year with greatest incidence in winter or spring 
and lowest Incidence in the last three months of the year. Usually the 
highest monthly incidence is not more than three times the lowest monthly 
incidence. 
Race and Sex - All races are susceptible. The Incidence is about 
equal in the two sexes but the mortality is higher in females. 
Age Incidence - There is little if any inherited passive immunity 
in young infants. Among 10,000 cases Investigated by Luttinger in New 
York the following age Incidence and the following percentage distribution 
of deaths from whooping cough were found. Age 
Percentage 
of cases 
Percentage of total 
whooping cough deaths 
1st year 
20 
51 
2nd year 
20 
2? 
3rd - 3th years 
1+0 
18 
6th - 15th years 
18 
3 
16 years and over 
2 
1 
Thus 80 percent of the cases and 96 percent of the deaths occurred under 
five years of age. This indicates that whooping cough is primarily a disease 
of very early childhood and that It Is much more dangerous under one year 
of age than at any other period. Seventy-eight per cent of adults are said 
to have had clinical whooping cough. 
Mortality - Half of the deaths from whooping cough occur under one 
year of age, 78 per cent under two years of age. The general case fatality 
rate is less than one per cent. Accurate mortality statistics are difficult 
to obtain because many deaths attributable,to whooping cough are reported 
as due to bronchopneumonia. Godfrey in New York State found that only 
65 per cent of the deaths due to whooping cough were reported as such. 
There are probably about 10,000 deaths per year from whooping cough in the 
United States. The rural death rate is somewhat highertthan the urban death 
rate, due to poorer nursing care and therefore a higher incidence of 
pneumonia. In New York Luttinger found a case fatality rate of per 
cent among tenement families and no deaths among cases attended by private 
practitioners. The tenement families in which deaths occurred all had 
more than three children, and most of the mothers went out to work during 
the day. 
Incubation Period and Course - Incubation period usually 7 to 10 days. 
Catarrhal stage lasts about 10 days, the spasmodic stage about one month 
with a range from one week to three months. The period of decline usually 
lasts three weeks, but may be indefinitely prolonged. Some cases never 
develop a whoop but may be infectious. This is particularly true of adults 
suffering from a second attack. 
Period of Communicability - From the beginning of the catarrhal stage 
up to four weeks after the beginning of the whoop. Most infectious during 
the catarrhal stage with gradual diminution during the spasmodic stage. 
Cough plate examinations show a sharp drop in positive results after the 
fourth week. It is reasonably safe to release from quarantine at this 
time. Chronic carriers of the organism are unknown. 
Complications - Bronchopneumonia is the most Important. It is most 
frequent in the second or third week of the spasmodic stage but may occur 
earlier or later. Early bronchopneumonia may be due to H. pertussis itself 
invading the lung tissue. Later cases are caused more often by secondary 
Invaders such as the hemolytic streptococcus or the pneumococcus. Otitis 
media occurs in about 7 Per cent of the cases. Diarrhea is a common complication during the summer. Gastric tetany may occur due to alkalosis 
from the vomiting of the acid gastric contents. Meningismus, meningitis, 
encephalitis, cerebral hemorrhage, emphysema (vesicular or subcutaneous) 
bronchiectasis, or hernia may occur. A tuberculous infection often develops 
into clinical tuberculosis following the disease. This should always be 
suspected in protracted cases of whooping cough. 
Mode of Transmlssion- 
(1) Droplet infection is the most important. The patient is dangerous 
within a distance of five feet. Infectiousness JLs greater than scarlet 
fever or diphtheria, less than measles or Influenza. 
(2) Direct contact by fingers. 
(3) Fomltes such as handkerchiefs, toys, drinking cups, towels, etc. 
Immunity- There is little or no passive Inherited immunity. One 
attack usually confers permanent immunity, but some adults have been proved 
to have a second attack by the recovery of the organism on cough plates. 
These cases usually do not develop the whoop, and the disease goes unrecog- 
nized but may be source of Infection, This is often called "grandmother 
whooping cough". Some children develop immunity without a history of 
clinical whooping cough, probably as the result of mild infections. 
Complement fixing antibodies are developed during an attack and disappear 
after recovery. Attempts are being made to develop a skin test which will 
give evidence of sensitivity to the organism. The opsonocytophagic test 
is usually positive as immunity develops. These tests may prove to be 
valuable in establishing previous exposure and the Immunity status of groups, 
and in the diagnosis of obscure cases. 
Specific Immunization and Treatment - A vaccine has been developed 
which is represented principally in this country hy the Sauer vaccine, 
consisting of whole killed organisms. Sauer's vaccine must he prepared 
from recently isolated, ;,smooth" strains of H. pertussis grown on media 
containing human blood, It contains 10 "billion organisms per c. c. A 
total of 7 to 8 c.c. is given in three doses at weekly Intervals sub- 
cutaneously as follows: 
1. 0.5 to 1.0 c.c. in each arm 
2. 1.5 c.c. in each arm 
5. 1.5 c.c. in each arm 
Severe reactions are uncommon. Complement fixing antibodies appear in the 
blood in three to four weeks and persist at a high level for at least 
twelve weeks. Smaller doses of a similar vaccine are used in Denmark 
where vaccination is said to be safe except in newborn infants. Vaccina- 
tion should not be performed under one month of age, but should be given 
as soon as possible thereafter, as immunity is not developed until 3 to U months after inoculation. Harrison and co-workers of the United States 
Public Health Service have reported preliminary favorable results from 
the use of alum-precipitated commercial vaccine, giving one dose of 1 c.c. 
The results of vaccination in the prevention of whooping cough have met 
with conflicting results. In Denmark it is widely used and believed to 
be effective both in preventing the disease and in making it less severe 
after it occurs. Public health agencies in the United States have not 
adopted the vaccine as a general procedure, but it is used rather exten- 
sively in private practice. 
The use of vaccine after the onset of symptoms is also believed to 
give favorable results in Denmark, It is not looked upon so favorably in 
the United States, but there are many observations in which severe cough 
and vomiting have been relieved following the use of vaccine. There is no 
evidence of the efficacy of immune horse serum for treatment of cases. 
Madsen states that convalescent human serum may be of some value in the 
early catarrhal stage. It has not been found of value as a prophylactic 
agent. 
Prevention and Control 
(l) Prevention of infection. The following points are important: 
(a) Early reporting of all cases. This is the responsibility 
of physicians, but since many cases are not seen by physicians, health 
officers should attempt to obtain reporting from all possible sources. 
In the presence of an epidemic, any persistent cough should be suspected 
of being whooping cough. 
(b) Early diagnosis, preferably by the cough-plate method. This 
can be done in cities where laboratories are near at hand. 
(c) Isolation of cases from susceptible children, especially 
those under five years of age. Cases or susceptibles should be removed to 
separate houses if possible. 
(d) Placarding of houses may or may not be advisable 
(e) Avoiding crowds in the presence of an epidemic. 
(f) Dally inspection of school children for catarrhal symptoms. 
School should not be closed. School children known to have been exposed 
may be excluded from the hth to l6th day after exposure. 
(g) Concurrent and terminal disinfection in the family is 
necessary only if young susceptibles are present. 
(h) Quarantine for four weeks after onset of whoop. (l) Vaccination. 
(2) Prevention of Death. 
(a) Postpone the disease until after five years of age. 
(h) Careful nursing with constant attendance night and day. 
(c) Avoid promiscuous contact of patient with others to avoid 
secondary infecting organisms which might cause pneumonia. 
(d) In good weather keep child out of doors or in fresh air as 
much as possible. 
(e) Keep up nutrition; counteract vomiting by frequent small 
meals easily digested and with little residue. 
(f) Supervision of the case by a physician. 
(g) Education of parents as to proper care of patient. 
(h) Extension of public health nursing service to provide 
education and supervision of families with young children. YEARS OF AGE 
DEATHS FROM INFLUENZA IN TEAAS 
IN 1938 
BY AGE 
TOTAL DEATHS-1612 
KEY-EACH MAJOR GRID 
REPRESENTS 20 DEATHS INFLUENZA 
1. Recognition of the disease.-- Whether occurring in a pandemic, in 
endemic-epidemic Incidence, or as sporadic cases this disease is 
characterized in its typical form hy sudden onset, fever of 1 to 7 
day's duration, accompanied hy excessive prostration, aches and 
pains in hack and limbs, coryza and bronchitis, and not uncommonly 
hy pneumonia as a complication. During epidemics when such cases 
occur in large numbers and over a wide area, other cases of less 
distinctive type are found to he epidemiologically related to typical 
cases, and in these the diagnosis would not he made without such 
obvious association. The clinical criteria of influenza are quite 
Indefinite, particularly in absence of widespread prevalence of the 
disease. Microscopic or other laboratory procedures are of no prac- 
tical value in determining or excluding the diagnosis of Influenza. 
2. Etiological agent. A filterable virus; associated often with various 
types of bacteria as secondary invaders. 
5. Source of infection. -- Probably discharges from the mouth and nose 
of Infected persons and articles freshly soiled by such disfcharges. 
I*. Mode of transmission. -- Believed to be by direct contact, by droplet 
infection, or by articles freshly soiled with discharges of the nose 
and throat of infected persons. 
5. Incubation period. -- Short, usually 2h to 72 hours. 
6. Period of communicability. -- Undetermined; possibly in prodromal as 
well as in the febrile stage stages. 
7. Susceptibility and immunity. -- Susceptibility is not general, for 
natural resistance or relative immunity appears to protect from 
one-quarter to three-quarters of persons Intimately exposed to the 
disease even during widespread epidemics. Acquired immunity if it is 
actually developed by an attack of and recovery from the disease is 
of short duration (a few months) and of low grade, or perhaps only 
effective against a certain strain or strains of the virus. 
8. Prevalence. -- Uncertain in pandemic, local epidemic, and sporadic 
occurrence, by reason of indefinite clinical symptoms. In epidemics 
may affect up to 50 percent of the population, especially at age groups 
between infancy and maturity. Commonly between December and May in 
North America. Occurs pandemically in cycles with intervals of several 
decades. 9. Method of control: 
A. The infected individual, contacts and environment 
1. Recognition of the disease and reporting: By clinical symptoms 
only. Uncertain in Interepidemic periods. 
2. Isolation: During acute stage of the disease, especially 
in severe cases and those complicated hy pneumonia. 
3- Concurrent disinfection: Discharges from the nose and throat 
of the patient. 
Terminal disinfection: None. 
5. Quarantine; None, hut visiting should he discouraged. 
6. Immunization: None. 
7. Investigation of source of Infection: Of no practical value 
B. General measures: 
1. During epidemics efforts should he made to reduce opportunities 
for direct contact infection, as in crowded halls, stores, 
and street cars. Kissing, the use of common towels, glasses, 
eating utensils, or toilet articles should he avoided. In 
isolated towns and institutions infection has been delayed 
and sometimes avoided hy strict exclusion of visitors from 
already infected communities. The closing of the public, 
parochial, and private schools has not been effective in 
checking the spread of infection. The Judicious use of masks 
hy nurses and other attendants may prove of value in preventing 
infection in hospitals, Scrupuloufe cleanliness of dishes 
and utensils used in preparing and serving food in public 
eating places should he required, Including the subjection of 
such articles to disinfection in hot soap suds. In groups 
which can he brought under daily professional inspection, the 
isolation of early and suspicious cases of respiratory tract 
inflammation, particuarly when accompanied hy a rise in 
temperature, may delay the spread of the disease. To mini- 
mize the severity of the disease, and to protect the patient 
from secondary infections and thus reduce mortality, patients 
should go to bed at the beginning of an attack, and not 
return to work without the approval of their physician. 
2. Crowding of teds in hospitals and institutions to accommodate 
increased numbers of patients and other inmates is to be espe- 
cially avoided. Increased spacing between beds in wards and 
dormitories should be carried out to reduce the risk of 
attack, and of the occurrence of pneumonia. YEARS OF AGE 
DEATHS FROM SCARLET FEVER IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-3I 
KEY -EACH MAJOR GRID 
REPRESENTS / DEATH SCARLET FEVER 
Throat infections caused by hemolytic streptococci may he divided into 
two general groups, (a) those associated with a scarlatinaform skin eruption 
and (h) those not associated with a skin eruption. There are many strains 
of hemolytic streptococci, some of which produce an erythrogenic soluble 
exotoxin. 
Scarlet fever was differentiated from measles by Ingrassius in Italy 
in 1560. First given its name by Sydenham in England in 1665. First recorded 
severe epidemic occurred in New Hampshire and Massachusetts in 1735. 
Streptococci were first Isolated from scarlet fever by Klein in 1885 and 
found to be present in most cases by Baglnsky and Sommerfeld in 1900. 
Since 1920 the work of many investigators, especially Dochez and George and 
Gladys Dick, points almost conclusively to the hemolytic streptococcus as 
the cause of scarlet fever. The evidence in favor of this point of view may 
be summarized as follows; 
(l) The hemolytic streptococcus can be recovered from nearly 100 per 
cent of cases of scarlet fever in the acute eruptive stage. Scarlet fever 
can be reproduced in susceptible persons by swabbing the throat with hemo- 
lytic streptococci. 
(2) The organism produces a soluble exotoxln which, when Injected 
intradermally into susceptible individuals, provokes a skin reaction known 
as the Dick test and fails in those who are immune. The toxin is neutralized 
in vitro by the serum of convalescent scarlet fever patients. 
(5) In response to toxin injections the horse elaborates an antitoxin 
which neutralizes the toxin _in vitro, gives the Schultz-Charlton blanching 
effect in scarlet fever rashes, produces a passive immunity to scarlet fever 
in exposed susceptlbles, and has a specific therapeutic action when injected 
in the early stage of the disease. 
(U) Injection of toxin into human subjects may produce a reaction 
Indistinguishable from a mild attack of scarlet fever, and by suitably 
grading the doses of toxin, an active immunity to scarlet fever is induced 
Incidence 
Scarlet fever is most prevalent in the temperate zone, especially in 
colder regions, but not in the Artie zone. It is primarily a cold weather 
disease, but epidemics may extend through the summer. Incidence has remained 
about the same for the past forty years in the United States, higher rates 
occurring Irregularly every few years. The seasons have no effect upon its 
virulence, i.e., the case fatality rate is about the same the year round. 
In hot climates scarlet fever is rare, and hemolytic streptococci are rarely 
found in throat cultures. The disease is milder in the southern than in the 
northern part of the United States. reason In United States, maximum incidence for northern states in 
January, for southern states October to November; minimum for northern 
states August, for southern states June to July. 
Age - Incidence low in first year, rapidly increases up to sixth year, 
then falls more gradually to twentieth yeah, after which it remains very J^ow 
Susceptibility - Zingher, in New York, demonstrated that susceptibility 
to scarlet fever as determined by,the Dick test Increased from the fifth 
month of life onward and was greatest in the one to two-year period when 
over 70 per cent of children were susceptible In the age group over 20 
years the percentage of susceptibles was reduced to about 18 per cent. He 
also found marked differences in susceptibility according to social status, 
children in the better class of homes yielding a susceptibility rate of 83 
per cent as against a rate of 22 per cent among children from poor homes. 
Urban groups are less susceptible than rural groups. Groups in institutions 
are usually less susceptible than the general population. 
Sex and Race- Slight excess of males up to six years. Marked excess 
of females above seven years. This is probably due to greater exposure of 
females in higher age groups because they nurse the cases. The Incidence 
among whites is three times as great as among negroes. This is due in all 
probability to missed and unreported cases in negroes, but there may be a 
relative racial immunity. 
Mortality - has fallen in the past years from i+0 to 2 per 100,000. 
Fifty-two per cent of deaths occur under the age of 5 years and 80 per cent 
occur under the age of 10 years For all ages the case fatality is 20 per 
cent higher among males. 
Case fatality -(i.e., percentage of fatal cases among total cases) has 
gradually been falling for the past years in most of Europe and in America 
(Sweden i860, 17 per cent; 1920, 1.9 per cent). The case fatality rate 
averages about 2 per cent at the present time and is higher for the age 
periods under five years In Russia, Poland, Bulgaria, Hungary, Italy, 
and China the fatality has remained higher. In Japan it is decreasing but 
is still higher than in America. It appears that the case fatality in 
general is lowest in places where quarantine is best carried out. Chapin 
(1926) believes that this is because the more virulent strains are being 
weeded out by quarantine He believes that strains which are usually less 
virulent may occasionally Increase in virulence, but that in well super- 
vised communities they are soon eliminated. The non-vlrulent strains persist 
because of mild and missed cases. The mortality rate averages 2-5 per 
100,000, which is lower than the rate of other acute infections. 
Incubation period - One to seven days, usually two to five days. 
Modes of Transmission - The organisms causing scarlet fever usually 
enter and leave the body through the mouth and nose. The discharges from 
draining sinuses and abscesses also contain the infectious agent. Strep- 
tococci may also enter the body through wounds and burns (surgical scarlet 
fever), and the uterus during the puerperium. The human is the only source 
of scarlet fever. The disease may be transmitted either by: (l) Direct contact, "by droplet infection, from typical or atypical 
cases of the disease. The clinical manifestations of scarlet fever are more 
varied than those of any other communicable disease. All degrees of severity 
of scarlet fever may he seen from mild upper respiratory infections or sore 
throat without a rash to fulminating eptlc or hemorrhagic cases. 
(2) Indirect contact with contaminated articles, linen, hands, 
infectious discharges, and food, especially milk. It is probable that the 
hemolytic streptococcus of scarlet fever can live longer outside the body 
of the host on fomites than most organisms. Milk becomes infected from 
human sources, usually a milk handler excreting hemolytic streptococci, 
either in convalescence from scarlet fever or as a mild or missed case. 
The cow's udder may become infected and act as a culture medium. Many 
extensive milk-borne epidemics of scarlet fever have occurred. The occur- 
rence of a number of cases of scarlet fever almost simultaneously in a 
community usually indicates that milk is the source of infection. Milk- 
borne epidemics of scarlet fever may occur at any time during the year. 
"Return cases" are those occurring in a patient's family soon after 
his recovery. They are more frequent after isolation periods under three 
weeks, but even after 9 weeks' isolation one per cent give rise to return 
cases. 
Period of Communicability and Carrier Problem - Depends entirely upon 
the presence of streptococci in discharges of patient. Nicholls (1927) 
cultured throats of cases at end of 3 weeks and of six coses at the end 
of four weeks and found all of them to harbor S. scarlatinas. Two out of 
three still harbored the organism at the end of five weeks. Gordon (1927) 
in a series of cases discharged on the twenty-first day or later found that 
6k per cent of cases not treated with antitoxic serum still harbored hemolytic 
streptococci, while only 38 per cent of treated cases harbored them. Of 
the severe untreated cases 68 per cent were positive on discharge; of the 
mild untreated cases 11 per cent were positive. 
Gordon states that the number of infecting cases varies inversely with 
the age of the patients; that is because of the fact that young children are 
more likely to develop one or more complications and continue to excrete 
the organisms, usually the throat, ears, suppurating glands, nose, or sinuses. 
A nasal discharge is especially dangerous and is least suspected of being 
infectious. A "return case" contracted from one of mild type is frequently 
characterized by unusual severity, and vice versa. 
Recognition of the fact that carriers of scarlet fever streptococci 
exists affords an explanation of recurrent outbreaks in schools and institu- 
tions, and sporadic cases with no known scarletinal contact. Milk-borne 
epidemics sometimes appear to have been started by carriers. There are so 
many strains of hemolytic streptococci that the detection of carriers of the 
scarlet fever strain is more difficult than diphtheria, typhoid, or 
meningococcus Infections, Both convalescent and contact carriers may be 
present in a community. Carriers of more than three months' duration are 
rare. Carriers of scarletinal streptococci usually have a negative Dick test so that an immune person may harbor these organisms. Jones has found 
that when the prevalence of scarlet fever increases the percentage of healthy 
carriers Increases greatly. This is similar to what has "been found in con- 
nection with the meningococcus. The increase of cases is the result of 
widespread dissemination of the organisms. 
The handling of carriers is a difficult problem. On discharge from 
the hospital, as a matter of precaution, it is best to advise patients to 
spend a week or two in the open air, to avoid intimate contact, especially 
with children, and to regard any recurrence of nasal discharge or catarrhal 
secretions from the upper respiratory tract as dangerous. 
Immunity - One attack of scarlet fever usually produces a permanent 
immunity. Second attacks occur in about one per cent of the individuals 
who have had scarlet fever. In one series of 5>000 cases there were 25 
relapses, 15 of which occurred within 30-55 days of the original attack. 
Control and Prevention 
A. General Measures: 
1. Early diagnosis - Often difficult due to absence of rash. In 
differential diagnosis of scarlet fever, the following diseases should be 
kept in mind: rubeola, rubella, diphtheria, exfoliative dermatitis, food, 
serum, and drug rashes. The Schultz-Charlton skin blanching test is useful 
when the rash is present. It consists of an injection of 0.1 - 0.2 c.c. 
scarlet fever antitoxin or convalescent serum intradermally into a portion 
of the body where the eruption is distinct (usually the abdomen). If the 
test is positive, there will be an area of blanching about cm. in diameter. 
Blake reports that in undoubted cases of scarlet fever blanching occurred 
in 80 per cent and that a positive test occurs more frequently when the rash 
is diffuse rather than punctuate. He states that the average Interval between 
the test and blanching was fourteen and a half hours, the shortest being 
six ana. a half hours. It may be as long as thirty-six hours. The absence of 
blanching does not exclude the diagnosis if characteristic symptoms and 
signs are present. 
The Dick test becomes negative during convalescence in a majority of 
cases, though in some instances it remains positive indefinitely. 
It is difficult to determine with certainty by bacteriological methods 
the particular hemolytic streptococcus of scarlet fever. Nevertheless throat 
cultures should be taken. The presence of such organisms in relatively 
large numbers in pure culture gives support to the diagnosis of scarlet 
fever and helps to rule out the possibility of diphtheria. 
(2) Notification - This is required immediately and on weekly report 
cards. Investigation of cases by the local health officer to determine the 
source of Infection and contacts. Placarding is advisable. (3) Isolation - Hospitalization is advisable in severe cases and where 
the case cannot he properly isolated at home. It is also advisable where 
there are many young children in the home. It is unnecessary in milder 
cases where proper isolation can be provided at home and where there is good 
cooperation between the medical attendant and the health authorities. 
Quarantine of contacts - Exclusion of food handlers from work until 
seven days have elapsed since last exposure to a recognized case. Swabbing 
of the throats of contacts may be done to determine the presence of hemo- 
lytic streptococci. No one except the nurse or attendant should come in con- 
tact with the patient. Adults, not in association with the patient, whose 
occupation does not bring them in contact with children or the handling of 
milk or food may be given a permit to enter and leave the premises. Children 
who are not immune as shown by the Dick test may be removed and quarantined 
in another household where there are no children for a period of seven days 
and then released and may return to school, but may not return to their homes 
until the patient has been released from Isolation. Susceptible children 
who remain in the house with a case must stay in quarantine until the patient 
is released from isolation. 
(5) Concurrent Disinfection - All articles which have been in contact 
with a patient and all articles soiled with discharges from the patient should 
be destroyed or sterilized. 
(6) Release - Three to four weeks from the onset of the disease is long 
enough in uncomplicated cases. It is no longer considered that the scales 
from the desquamating skin contain the infectious agent. Patients should 
not be released if there is an complication- suppurative process, or nasal 
discharge. Since post-scarletinal nephritis may occur during the third or 
fourth week, it is well to keep the patient in bed or restricted for four 
weeks, and isolation is the simplest means of encouraging this. Three negative 
throat and nose cultures for hemolytic streptococci before release should 
be of advantage in minimizing return cases, but this is practicable only in 
hospitals. Even there it is not practicable to identify the organism as a 
scarlet fever strain. In cases having a complicating discharge, however, 
three negative cultures should be required for release from quarantine. 
(7) Terminal Disinfection - Thorough cleaning of the room and its con 
tents is required. 
(8) Supervision of milk supply - Careful supervision of the production 
of raw milk supplies is essential but will not prevent epidemics. Pasteuriza- 
tion of milk is the only safe preventive measure. 
B. Specific Measures 
(l) The Dick test - This test determines susceptibility to scarlet 
fever. It is performed by the intradermal injection of 0.1 c.c. of the toxin 
of the S. scarletinae grown form k - 6 days in a broth culture. The amount of toxin injected is known as one skin test dose (S.T.D.): that is, the 
smallest amount toxin which will produce a positive Dick reaction in known 
susceptible individuals and a negative reaction in immunes. 
The toxin is usually Injected on the flexor aspect of the forearm and 
must he read within 2k hours. A positive Dick test consists of an area of 
erythema 10 mm. or more in any diameter at the site of injection. There 
is usually no swelling or induration associated with a positive reaction 
as is found in a positive Schick test. The Dicks state that there is some 
correlation between the intenseness and size of the reaction with the degree 
of susceptibility of the patient. 
Pseudo reactions resulting from sensitization to the protein in the 
test material may occur, especially in older children and adults. A 
control test should be made in dealing with the above groups (older children 
and adults) with the toxin heated for a long period as it is heat stable. 
The Dicks claim a high degree of precision for this test and report 
one group of 22,856 Dick negatives who have passed through one or more 
epidemics of scarlet fever without contracting the disease. They also 
report another group of 2,557 nurses and interns with negative reactions 
who were constantly exposed to scarlet fever and remained immune. Others, 
however, have occasionally encountered scarlet fever in supposedly immune 
persons. The test is of practical value in institutions for children where 
Immunization is contemplated, and in families where a case of scarlet fever 
has occurred. 
(2) Immunization - (a) Active. This consists of the subcutaneous 
injection of scarlet fever streptococcus toxin in five Increasing doses at 
weekly intervals, namely, 500, 2,000, 8,000, and 80,000 S.T.D. 
The patient should be given a Dick test one month after the last injection. 
If the test is negative the patient, is probably, immunized. If the test is 
positive, an additional dose of 90,000 S.T.D. shoiid be given and a retest 
done one month later. This series of injections is usually without danger 
but severe, unpleasant local and general reactions, including erythematous 
rashes, occur occasionally. The Dicks claim that with this method 95 Per 
cent of susceptibles will become Dick negative within two weeks and 90 per 
cent will remain immune for one to five years. 
The development of a. toxoid comparable to the diphtheria toxoid has 
not yet been accomplished. Yeldee of the U. S. Public Health Service has 
separated the erythrogenlc factor of the toxin and precipitated it with 
tannic acid. Preliminary tests Indicate that this substance Injected intra- 
dermally will cause the Dick test to become negative, and that it rarely 
produces severe reactions. 
Due to the fact that scarlet fever is generally a mild disease with 
low case fatality, it is not considered advisable to advocate active 
Immunization against scarlet fever in the general population. There are, however, certain circumstances under which this procedure may he used with 
benefit. They are: 
(l) in epidemics 
(2) in certain family groups 
(3) in institutions caring for large groups of children, and 
(if) in personnel of hospitals. 
(b) Passive. Scarlet fever antitoxin or convalescent serum can be 
employed for this purpose in contacts where immediate protection is desired. 
The usual practice is to Inject 5 c.c. of scarlet fever antitoxin subcutaneous 
ly or intramuscularly. This gives immediate protection in a large per cent 
of cases but the duration of Immunity is short, probably no longer than two 
weeks. A dose of 10 c.c. of serum will probably protect for four weeks, but 
one should not rely on this as cases of the disease have been reported from 
six to seven days after this procedure. The production of passive immunity 
is of value under circumstances where there are cases under poor hygienic 
conditions, and where a number of small children are exposed and where 
isolation cannot be carried out. It is not advocated generally. If convales- 
cent serum is used, the dosage should be increased to two to three times 
that of the antitoxin. 
Since the advent of sulfanilamide the antitoxin and convalescent serum 
are usually reserved for the most severe type of case. While highly effective 
in treatment of scarlet fever, both are expensive, and the antitoxin often 
gives very unpleasant serum reactions. YEARS OF AGE 
DEATHS FROM MEASLES IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-114 
KEY -EACH MAJOR GRID 
REPRESENTS DEA THS MEASLES 
( RUBEOLA - MORBILLI) 
Measles is a specific infectious disease characterized by fever, 
catarrhal symptoms, an exanthem and desquamation. 
Historical - The first definite mention of measles was made by an 
Arabian physician about 900 A.D. The disease was at first considered a 
variety of smallpox, and it was not until the seventeenth century that it 
was recognized as a distinct clinical entity. Much of our present know- 
ledge is due to the work of Panum who studied the disease in the Faroe 
Islands in 18*4-6, where it had not existed for 65 years. 
Etiology - The etiological agent at the present time is considered 
to be a filterable virus. Experimental work, however, has been carried on 
without the specific causative agent being discovered. Innoculatlon of 
animals and humans with blood and nasal secretions from patients have pro- 
duced the disease. Various bacilli, cocci, and protozoa have been indicated 
The virus is present in the blood and nasopharyngeal secretions from one to 
two days before rash appears. Virulence Increases as incidence of the dis- 
ease increases. 
Immunity - Natural immunity is rare. There is a universal suscepti- 
bility to the disease. 
Prevalence - The disease has universal distribution. It may be 
endemic, but epidemics tend to occur every two years with the appearance 
of large numbers of susceptible people. It ranks next to smallpox and 
Influenza in degree of contagiousness. Epidemics are common in urban com- 
munities . 
Age Incidence - All ages are susceptible. Intra-uterine Infection 
has been reported. It has been estimated that approximately 90 per cent 
of all persons surviving to the twentieth year of life have had measles. 
The disease is most prevalent in the age groups five to nine and ten to 
fourteen; 75 to 80 per cent of cases occur before the fifth year but this 
is probably not correct as such cases are not as well reported as those of 
older children. 
Mortality - Measles is rarely fatal per se. Death is usually due to 
complications. The total mortality reported from the U. S. Registration 
Area varies roughly from 2,500 to 8,500 deaths yearly or 5 to 10 per 
100,000. A fatal outcome in measles is due mainly to complications, the 
most important of which is pneumonia, since approximately 95 Per cent of 
the deaths associated with measles results from pneumonia. The relation- 
ship between measles and pneumonia was shown during the World War by 
Vaughan who made the following statement in regard to this: 
”(l) Of every thousand men with measles, *+*+ had pneumonia and 19 died. (2) Of every thousand men without measles, 17 had pneumonia and 
2 died. 
(3) A person who has recently had measles is ten times more likely 
to die from pneumonia than is the person who has not recently 
had measles." 
In considering the question of mortality from measles, superimposed 
infection should he mentioned as another factor which produces death. The 
possibility that a tuberculous focus may be awakened to activity as a re- 
sult of measles should always be considered as a remote cause of mortality 
from measles. There is no sex predisposition. 
Measles is a disease that should not he hospitalized except in case of 
actual complication. Experience has shown that the incidence of complica- 
tions is greatly Increased where measles cases are uniformly sent to isola- 
tion hospitals. This is probably due to interchange of pathogenic organ- 
isms, or places the individual in contact with organisms which are not 
natural flora in his own respiratory system. 
Case Fatality Rate - Fatality rates for all persons attacked are 
probably not over 3 or per thousand cases. It varies greatly with age, 
physical condition and social and environmental conditions. Fatality rates 
up to 35 per cent have been noted in Infant asylum outbreaks, due to the 
enhancement of the usual risk in young children by the prevalence of 
rickets and other forms of malnutrition, the overcrowding and inadequate 
nursing and hygienic care. In whatever degree these factors operate in com- 
munity life, they serve to increase the fatality rates. The fatality rates 
by age probably approximate 30 - 50 per thousand cases in children under 
one year old; 15 - 30 per thousand at age one; 10 - 15 at age two. Between 
five and fourteen the fatality rate is probably not more than 2 per thousand 
gradually increasing in adult life to approach in old age the rates of 
early childhood. 
Racial Distribution - Measles attacks all races. 
Seasonal Incidence - Measles is more common in winter and spring. Inci- 
dence increases in cold weather. In the U. S. the greatest prevalence is 
from March to June, 
Incubation Period - days. Rash appears from 13-lk days after in- 
faction. When convalescent serum has been used, the incubation period may 
be prolonged, in some instances up to 21 days. 
Period of Communicability -From onset of catarrhal symptoms to the 
disappearance of the eruption. It is infectious during pre-eruptive stage. 
Five days before and five after eruption appears is the most highly infec- 
tious period of the disease. Mode of Transmission 
(l) Close proximity and direct contact is the most important. The 
infectious agent is disseminated hy minute droplets given off during cough 
ing or sneezing. 
(2) Indirect contact. Short exposure during period of communicahility 
will 'suffice for transmission. A carrier state is not known to exist. 
Control Measures 
(l) Early diagnosis - Koplik's spots - rise in temperature - edema of 
conjunctiva - catarrhal symptoms. 
(2) Isolation of cases and contacts for 16 days should be practiced 
though only 7 to 10 per cent of the population will be protected by this 
procedure. Sir Arthur Newsholme believes "that the measles problem is very 
similar to the influenza problem. In both, so far as our present knowledge 
goes, the chief hope of saving life lies in the preventing or in diminishing 
the mortality from streptococcal or pneumococcal pneumonia in the disease." 
The primary benefit resulting from isolation of patients is to reduce pro- 
miscuous contact and likelihood of secondary Infection. In hospitals and 
institutions both uncomplicated and complicated cases should be strictly 
Isolated. If measles appears in an institution which cares for young child- 
ren or if measles is present in a community where such an institution is 
present, quarantine of the Institution may be of some value in preventing 
the introduction of measles. 
(3) Concurrent and terminal disinfection. 
{k) Schools should not be closed. 
(5) Education of public as to the seriousness of the disease. 
(6) Prompt and complete reporting of cases 
(7) Care of the eyes 
(8) Special measures should be designed primarily to reduce mortality. 
Infants in asylums should be kept in best possible condition, special atten- 
tion being given to prevention and cure of rickets. Such institutions should 
in effect be quarantined during outbreaks .in vicinity, and if invaded, spe- 
cial attention should be to care of* those attacked.’ Convalescent serum, 
should be given,.if available, to children under three, but should not be 
relied upon alone. With a potent serum the disease will usually either be 
modified or prevented. In the community at large, extra nursing personnel should 
be employed. Cases should be investigated to ascertain family contacts under 
three years of age so that the 'parents may be instructed in the particular danger of measles to these children and shown how best to arrange for the 
care of the sick and those who will probably come down later. Families in 
the neighborhood who have children of this age, or physically handicapped 
children, should also be visited and Instructed, and efforts made to im- 
prove physical condition if Impaired. Convalescent serum should be made 
available for use in suitable cases. Adequate medical and nursing care should 
be provided for the indigent, and in exceptional circumstances hospitaliza- 
tion should be provided. Cases should be isolated for their own protection. 
Proper rest during and after an attack is of great Importance in pre- 
venting sequelae. The patient should go to bed on the eighth day after 
exposure and remain in bed until all dangers for complications are past. 
The prevention of tuberculosis following an attack of measles is one of the 
most important points to be emphasized. 
Prevention - Exposed people can be passively Immunized for two to four 
weeks with convalescent serum taken from a person who has had measles pre- 
ferably six to ten days after recovery. Convalescent serum may be taken 
as long as four months after recovery. A dosage of 5-10 c.c. may prevent 
disease or cause the disease to be milder. Its use is particularly desir- 
able in very young or debilitated children. 
The following is a brief review of the literature on the prophylactic 
use of immune serum: 
1. In 1915, Doctor Charles Herman, New York City, rubbed nasal secre- 
tions from patients on nasal mucous membrane of non-immune children. Pro- 
duced modified disease. 
2. First successful immunization with convalescent serum done by 
Nlcolle and Conseil in 1916. 
5. Von Torday immunized 2,000 exposed children - only 3 per cent were 
not protected to some extent. 
4. Debre and Ravina injected convalescent serum from 7-10 days after 
exposure; complete protection not brought about but produced mild disease 
as evidenced by prolonged incubation period; suppression of invasion symn- 
toms; slight fever; absence of catarrhal symptoms and Kopllk's spots, faint 
eruption; short course; mild or no constitutional symptoms. 
5. Degkwltz was first to use whole adult blood of donors who had had 
measles. Eeltschel and Zlngher Independently used serum or whole blood 
from Immune adults and found that some protection was derived from this 
method but that dosage had to be increased. 
6. Optimum time for obtaining convalescent serum is 6 to 10 days 
after patient's temperature has reached normal. 
7- Convalescent serum can be kept as long as six months 8. Dosage for complete protection. Children up to 3 years of age not 
exposed more than k days - 2.5 c.c.j if exposed from 5 to 6 days - 5 c.c.; 
7.5 c.c.; if exposed for 7 days; larger doses for older children. After 
8th day of exposure, disease may not he prevented hy infection of immune 
serum hut may he modified. Whole hlood instead of serum may he used in 
double the above dose. 
9. To cause modified measles, Zingher advocates the following methods 
from fifth to tenth day after exposure; 2.5 c.c. of convalescent serum; 
5 c.c. serum from brother or sister who has had the disease or 10 c.c. of 
adult immune serum. 
10. Convalescent serum or adult whole hlood is not effective when used 
therapeutically. 
11. Use of prophylactic serum indicated in 
(a) children in first four years of life, 
(h) children suspected of having tuberculosis, 
(c) children who have other contagious diseases, especially in 
hospitals and in other institutions, and 
(d) in other instances where the health, age and environmental 
circumstances make the disease dangerous. 
McKhann and Coady have reported on the possibilities of preparing ex- 
tracts of the placenta which might he used in protecting infants and children 
against certain diseases. These workers made a two per cent sodium chloride 
extract of several placentas and precipitated the globulins with ammonium 
sulphate. The ammonium sulphate was removed hy dialysis. The solution which 
remained after this procedure was passed through a Berkfeld filter and upon 
injection into animals was found not to produce any harmful effect upon the 
tissues. Upon qualitative determination, such a placental extract: 
(l) neutralized diphtheria toxin, 
(2) blanched scarlet fever rashes, 
(5) neutralized poliomyelitis virus, and 
{k) prevented measles in exposed susceptible patients 
They have reported results with this extract comparable with those ob- 
tained with human convalescent serum both in the prevention and modifica- 
tion of the clinical attack of measles. This work is well confirmed, and 
will be of great value in producing passive immunity against measles and 
modifying the disease under suitable circumstances and it will be possible 
to have sufficient quantities of the material for general use. Y EARS OF AGE 
DEATHS FROM TUBERCULOSIS IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-4,111 
KEY -EACH MAJOR GRID 
REPRESENTS 50 DEATHS TUT RCULOSIS 
—t 
Evidence of past or present infection in the absence of clinical 
symptoms can he determined hy a variety of specific tuberculin reactions, 
among which the Mantoux intradermal test is the most reliable. In 
the presence of early constitutional symptoms with or without pulmonary 
signs, the existence or location of pulmonary or other thoracic lesions 
can best be revealed by X-ray. When fever, cough, loss of appetite and 
weight and physical signs or ausculation and percussion are found, the 
pulmonary lesion is already well developed. Discovery of the tubercle 
bacille in the sputum confirms the diagnosis not infrequently in early 
cases but is an evidence usually of a weld advanced lesion. 
Pulmonary tuberculosis is caused by the human type tubercle bacilli, 
although the bovine type has been isolated from pulmonary lesions in 
man. 
Source of infection. -- The specific micro-organism present in 
the discharges, or articles freshly soiled ftom the discharges from any 
open tuberculosis lesions, the most important discharge being sputum. 
Of less importance are discharges from the intestinal and genito-urinary 
tracts or from lesions of the lymph nodes, bone and skin. 
Mode of transmission. -- Usually through the discharges of the 
respiratory tract, by direct or indirect contact with infected persons, 
by means of coughing, sneezing or droplet infection, by kissing, by use 
of contaminated eating or cooking utensils and possibly by contaminated 
flies and dust. Infection rarely results from casual contact but usually 
results from continued exposure. 
During the year 1938 the greatest number of deaths from tubercu- 
losis in Texas occurred in young adults in the age group between twenty 
and thirty in both males and females. Comparison 6f the figures for 
the last few years show that there has been little change in the annual 
tuberculosis death rate as compared with the steady decline of many other 
states. The logical conclusion is that our position is stationary, and 
until our present plans have been fortified a plateau trend of rates is 
to be expected. A plan of attack was so well brought out by Dr. J. A. 
Myers, in a recent nine point control program for the United States, that 
it can be well repeated and applied to Texas. 
"The following procedures," he states, "directed by the medical 
profession and carried out by its members in cooperation with closely 
allied groups and an Informed public should suffice to control the 
disease: 
"1. Administer the tuberculin test to every one. 
"2. Make X-rays of the chests of all positive reactors approach- 
ing and beyond adolescence. "3. Make complete examinations of all whose X-rays present 
shadows which might be due to tuberculosis in order to arrive at the true 
diagnosis. 
"1+. Arrange for an adequate number of beds in private and public 
hospitals and sanatoriums so that all persons who have tubercle bacilli 
in their sputums which cannot be eliminated quickly can at once be re- 
moved from their homes, 
”5. Arrange to treat or keep under close observation all who 
have tuberculous lesions, the progressiveness or activity of which cannot 
be determined at once. The physician can manage the disease of the 
majority of such persons in the home. 
"6. Since tuberculosis is usually arrested, not cured, and is a 
relapsing disease, all persons whose disease is under control should be 
examined frequently. 
”7. Arrange for the protection of citizens against the importa- 
tion of persons with communicable tuberculosis by providing adequate 
examinations of all persons entering the country's ports and crossing its 
borders. Exercise the same precaustions for those of other nations by 
examining adequately this country's citizens before they leave its ports 
or cross its borders= 
M8. Support the veterinarians at every opportunity in their 
efforts to control the disease in animals, because it is transmissible 
to man. Their past accomplishments merit this and more. 
"9. Take an active part in local and national tuberculosis associa- 
tions, the local medical society, the American Medical Association and all 
other organizations engaged in tuberculosis work," 
Any tuberculosis program suggested would contain many of the pre- 
ceding nine points. They are not necessarily listed in the order of 
Importance. Any difference in opinion will be in how far these points 
can be carried out rather than their theoretical value. YEARS OF AGE 
DEATHS FROM DIPHTHERIA IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-233 
KEY -EACH MAJOR GRID 
REPRESENTS 5 DEATHS DIPHTHERIA 
Diphtheria is an acute infectious disease caused by the Klehs-Loeffler 
bacillus characterized pathologically by the formation of a pseudomembrane 
on some mucous surface, usually the oropharynx or nasopharynx. The surface 
of wounds may also become Infected, -A soluble toxin is elaborated which is 
absorbed and to which the symptoms and lesions of the disease are due. The 
bacillus itself may find its way into the blood and tissues, but the essen- 
tial factor in causing clinical manifestations of the disease is the soluble 
toxin. One attack does not give permanent immunity. 
Historical note. - Although it is a little more than one hundred years 
since diphtheria received its present name, the history of the disease can 
be traced to a remote period. It is doubtful if diphtheria was known in 
the time of Hippocrates, though certain passages Imputed to be his writings 
suggest that it was recognized at that time. It was not until the first 
century A. D. that an unmistakable description of diphtheria was given by 
Aretaeus of Cappadocia under the name of Egyptian or Syriac Ulcer, owing 
to its having originated in Egypt and Syria, thence spreading to all 
European countries. In 1885, Klebs described for the first time the bacil- 
lus now known to be the specific organism, and which was first cultivated 
in by Loeffler, hence the name Klebs-Loeffler bacillus. The work of 
Loeffler was confirmed by Roux and Yersln, who were not only able to 
produce paralysis in animals by inoculating them in the trachea and also 
subcutaneously with diphtheria bacilli, but also demonstrated the existence 
of a diphtheritic toxin. The toxin was obtained by filtering the culture 
fluid through porcelain. The discovery of diphtheria antitoxin was made 
in 1890 by Behrln and its practical value shown by Emile Roux in l89*+. The 
test of immunity to diphtheria was Introduced by Schick of Vienna in 191^. 
The use of toxin-antitoxin for immunization purposes, suggested by Theobold 
Smith in 1907, was first applied clinically by Behring in 1915- Its 
employment, however, on a large scale was due to the work of Park and Zingher 
(1917-1918) in the United States. 
Prevalence or Incidence of Diphtheria. - Diphtheria is most prevalent 
during childhood but no age is exempt The incidence of the disease is 
at least during the first year of life, and higherst from five to seven years 
of age. The greatest susceptibility to diphtheria is in the age group from 
one to five, and about 80 per cent of the deaths occur under five years of 
age. In the Death Registration Area of the United States in 1900 diphtheria 
death rate was 100,000. In 1952 the rate was Diphtheria is 
essentially an endemic disease, although it may become epidemic. The 
periodicity of diphtheria is indefinite. 
Causative Organism. - Diphtheria is due to the invasion of specific 
microorganism, the bacillus diphtherias (Klebs-Loeffler). The bacillus 
grows locally on mucous surfaces or on the skin. When kept in a dry state, 
under certain circumstances, the bacillus possesses considerable resistance. 
A culture may be obtained from a dry membrane under gertain conditions. The 
organism is very resistant to cold but is rapidly killed by heat, especially 
by the action of the sun's rays. It may be also readily destroyed by antiseptics (phenol, Hgclg). It grows best on Loeffler's medium at a 
temperature of 37 C. The dissemination of the bacillus in different 
parts of the body is rare and when so found is probably not of much 
pathological significance. The bacilli begin to disappear* from the site of 
the lesions as the acute symptoms subside so that by the end of a month 
about 85 per cent of diphtheria patients are free from bacilli and by the 
end of the second month usually 98 per cent; the- remainder may become 
chronic carriers. Some authorities maintain that the diminution of virulence 
precedes the disappearance of the organism, but most Investigators maintain 
that they retain their virulence throughout the course of the disease. 
Modes of Transmission. - Period of incubation may be from two to seven 
days, but the average is from three to five. The attack rate - on the 
average about 6.5 per cent of those exposed develop clinical diphtheria. 
The infective agent usually has its exit from the body in the secretions of 
the mouth and nose, and it also gains admission commonly through the mouth 
and nose. The source of infection in the spread of the disease is the case 
or carrier. The case may be typical, atypical, or mild. 'The "missed" 
case is potentially very dangerous. The infection is usually transmitted 
directly from one person to another, as by kissing or droplet infection in 
coughing, sneezing, and speaking. The bacillus may also be conveyed 
indirectly from one person to another in many ways, as for example, toys, 
pencils, food, fingers, spoons, cups, handkerchiefs, or any object on which 
may be found fresh secretion from a case or carrier. The latter mode of 
transmission is most common among children,, Personal hygiene should there- 
fore be emphasized as an important factor in the prevention of diphtheria. 
This is not a disease that is easily transmissible and is, therefore, more 
commonly spread from one person to another by direct contact. Experience 
clearly teaches that diphtheria 1s spread mainly by typical and atypical 
(abortive) cases, recent convalescents, mild and missed cases and carriers. 
Occasionally milk becomes contaminated, resulting in the spread of diphtheria 
It is claimed that domestic animals, especially pets, may transmit the infec- 
tion to a human being under exceptional circumstances. 
Diphtheria Carriers. - It is generally accepted that diphtheria con- 
tinues as a disease entity by means of chronic carriers who act as sources 
or reservoirs of infection and from these the organisms are spread under 
favorable conditions to susceptible individuals. It is conceded that 
diphtheria would not be much of a public health problem if it were not for 
"carriers". A possible carrier can be diagnosed without difficulty and the 
virulency of the organism found can be determined by laboratory tests. 
However, the treatment of the carrier offers the most difficult phase of the 
problem. 
Types of Carriers; 
1. Incubationary. These may play some part in the dissemination of 
the Infection, but the incubation period of diphtheria is so short that this 
would not be an important factor in its spread. 
2. Convalescent carriers. Virulence tests are not necessary in such 
carriers because it has been found that the organisms in 90 per cent of 
canvalescent carriers are virulent. Physical defects of the nose and throat 
predispose to the chronic carrier state. 3* Contact carriers. These occur among attendants, members of the 
family and contacts of cases and carriers in from 10 to 20 per cent of 
exposures. The organisms are virulent in 80 per cent of the contact carriers 
hut the condition is temporary unless there is some predisposing deformity 
or a chronic focus. These carriers are Immune in that they are Schick 
negative. In the general population true carriers of virulent organisms 
are less than one in one thousand. Among children about 2 per cent are 
carriers. Only about 10 per cent of non-contact or non-convalescent carriers 
show virulent organisms. 
k. Pseudo-carriers. In doing extensive carrier work, a number of persons 
will be found who are carrying organisms which morphologically resemble 
virulent diphtheria bacilli. Laboratory examinations show that many of 
these organisms are diphtheroids or non-virulent diphtheria bacilli. In 
dealing with these individuals it is desirable to determine whether the 
organisms are virulent and caution should be used in establishing long-term 
quarantine without doing the "virulent test". On the other hand, carriers 
of virulent bacilli should be isolated, appropriate treatment instituted. 
Release cultures should be made before determining the procedure that should 
be advised. 
Symptomatology, Diagnosis, and Complications. - This can be prepared by 
use of any standard textbook on medicine. 
Control of Diphtheria. - Important factors involved in the prevention 
and control of diphtheria are; 
1. Securing swabs and the microscopic examination of cultures from 
the throats of those who have been exposed to infection. 
2. The use of the Schick test. 
3. Production of active and passive immunity. 
U. The virulence test. 
5. Proper use of antitoxin in the treatment of the disease. These 
elements in the control program are mentioned specifically because of their 
value and in order to emphasize their use in dealing with diphtheria as 
a family and community problem. 
Is the prophylactic use of diphtheria antitoxin justified? The 
following statement is made by the Medical Research Council of England on 
the use of antitoxin in producing passive immunity and is essentially in 
accord with the attitude of the medical profession of the United States per- 
taining to this question: 
"When the outbreak occurs in a community which is not in close touch 
with medical observation and when the circumstances are such that the pro- 
bability of other cases occurring is great, then the use of antitoxin may be 
considered. Such instances will be confined to communities of children, 
since adults are so frequently immune naturally that the likelihood of other 
cases occurring is not so great. 
"It may be remarked that the prophylactic injection of antitoxin has 
certain objections both practical and theoretical. If a child develops diphtheria after the effect of the antitoxin has passed off, the therapeutic 
injection may possibly be rendered less effective owing to the presence of 
precipitins in the blood, and, possibly, may be rendered more toxic by the 
existence of an acquired hyper-susceptibllty to the horse serum. 
"The prophylactic injection of antitoxin should, therefore, be looked 
upon as a weapon for use in serious emergencies, which are rare, and even 
then as a palliative which may leave the state of emergency to develop 
again in three weeks. It will be a matter of individual consideration 
whether in any particular case it is not more satisfactory to proceed at 
once along the lines of separation and active immunization of susceptibles 
by means of Schick's test and toxin-antitoxin mixture rather than to estab- 
lish a sense of security which is sometimes false." 
Since this statement was published the use of toxoid has largely 
replaced the use of toxin-antitoxin. 
Active Immunization. 
1. Infants under six months are unsuitable for immunization owing to 
the frequent presence in their blood of antitoxin passively transmitted by 
the mother. 
2. Children between six months and five years should all be Immunized 
without a Schick test. 
3- Children of five years upon entering school, who have not been 
Immunized, and coming under the Influence of health officers for the first 
time should all be immunized without a Schick test, since most of them are 
susceptible. 
4, Older children up to fifteen years should be immunized only if the 
Schick reaction is positive, since in some schools the number of susceptibles 
is small and the immunes are likely to suffer more severe non-specific 
reactions after injection. 
5. Children over fifteen years, for the same reason, should be 
immunized only if the Schick reaction is positive. 
If the Schick test, carried out six months after immunization, is still 
positive, one or two further injections should be given and are usually 
sufficient to bring about the desired result 
In France in 1923, Ramon Introduced a new agent with which he proposed 
to produce active immunity. The agent he called "anatoxin" . English-speak- 
ing countries have substituted the word "toxoid" for "anatoxin", which 
prevents confusion in the use of antitoxin. Toxoid is produced by the 
detoxification of toxin by adding k c.c. of formaldehyde to 1000 c.c. of 
filtered toxin and heating it from three to six weeks at a temperature of 
from 30 °to C. This provides a product which is non-toxic and non- 
sensitizing but which retains its antigenic properties. 
Toxoid is given subcutaneously, usually in two or three doses with 
a two to four weeks' interval. In children under eight years of age the 
reaction, if any, following the Injection of toxoid is slight. However, 
after the age of eight a marked reaction may occur but without danger. 
Toxoid is uniformly used in France and Canada, and it is rapidly replacing 
toxin-antitoxin in the United States and other civilized countries. Toxoid has the following advantages as compared with toxin-antitoxin: 
1. It is about 30 per cent more effective even when only two doses 
are given. 
2. It contains no serum or other animal protein likely to sensitize 
to a later therapeutic serum injection. 
5. It is without local or general reaction in practically all children 
under seven years of age. Reaction in older children and adults are only 
unpleasant, not dangerous. 
It contains no free toxin. 
5. It is more stable, retaining its potency for a longer period and 
is not affected by freezing The expiration date is usually eighteen months 
and it may be longer. 
6. Immunity occurs much more rapidly (three to six weeks). 
7- It is easier to make and costs less 
Toxoid gives excellent results and deserves the attention of the 
health worker, and the physician particularly, since its use is followed 
by so little local or general disturbance in the age group with which we 
are most concerned in the prevention and control of diphtheria. 
Alum-precipitated toxoid possesses certain advantages and will probably 
partially replace the soluble or normal toxoid- This is obtained by adding 
alum potassium sulphate in the process of making toxoid, which combines 
with or is absorbed by the protein to form an Insoluble compound. The 
insolubility makes it possible to Inject larger quantities and as a result 
the antigenic property is prolonged. The presence of alum slows absorp- 
tion in the tissues. Only one dose of alum precipitated toxoid is usually 
used as it causes a high percentage of immunization. 
Disinfection, - Concurrent disinfection in the treatment of cases 
of carriers. Terminal disinfection. 
General measures which may be employed in the control of diphtheria, 
such as personal hygiene, supervision of milk supplies, and the education 
of the public should be kept in mind. Good oral hygiene is of Importance 
as a-means of preventing the spread of infection. 
A sore throat is always potentially dangerous. YEARS OF AGE 
DEATHS FROM POLIOMYELITIS IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-47 
KEY - EACH MAJOR GRID 
REPRESENTS / DEATH ACUTE ANTERIOR POLIOMYELITIS 
Definition - Poliomyelitis Is an acute infection, due to a filterable 
virus, occurring Loth in epidemic and sporadic form with a special tendency 
to localization in the anterior horns of the gray matter of the spinal 
cord; hence the name anterior poliomyelitis. Recent publications present 
the point of view that it may he a generalized infection, the central 
nervous system Involvement being secondary, but this has not been confirmed. 
Etiology - Epidemiological evidence first indicated that poliomyelitis 
is an infectious disease. Experimental evidence has confirmed this view. 
It is caused by a living virus. It passes through a filter and produces 
the disease when injected intracerebrally into monkeys. In 1909 Landsteiner 
and Popper succeeded in transmitting the disease to monkeys by using the 
spinal cord of a child who had died of poliomyelitis. Flexner and Lewis 
in the same year confirmed this result and extended the findings by trans- 
mitting the disease through several series of monkeys. 
The nature of the virus is unknown. It is present in greatest concen- 
tration and can be found in the spinal cord and brain of Infected animals 
and humans. It has been demonstrated in other organs; viz, the mucous 
membrane of the nose and pharynx, lymph nodes, and is said to have been 
isolated from the intestine. 
. o o 
The virus is killed by a temperature of to 50 C. in half an hour 
and by comparatively weak disinfectants. It is not destroyed by low tem- 
peratures nor by drying over caustic potash. The virus maintains its viru- 
lence in 50 per cent glycerine for long periods. 
Geographic Distribution - The area of geographic distribution of 
poliomyelitis is world-wide. There appears to be a tendency to somewhat 
higher prevalence of clinically recognizable cases in colder latitudes. 
The incidence of the disease decreases as the equator is approached, and 
in the tropics clinical poliomyelitis is a rare disease. 
Seasonal Prevalence - Poliomyelitis is usually a warm weather disease. 
In the United States about 75 per cent of the cases appear within the five 
months' period from July to November, Inclusive, with 50 per cent of the 
cases falling in the three months of August, September, and October. The 
curve rises in July and reaches its peak in August or early September and 
declines rapidly with the advent of cold weather. This is the usual seasonal 
distribution in endemic areas. Occasionally poliomyelitis will either 
remain prevalent or appear in the cold months of the year. In the regions 
south of the equator the seasonal prevalence is the reverse of that for the 
United States. 
Urban and Rural Distribution - According to Frost, one of the most 
definite characteristics of this disease is its tendency to higher incidence 
in thinly populated areas; hence, it is more prevalent in rural than urban 
areas. This is due to the fact that there is less chance for acquired 
immunity by exposure to repeated small doses of the virus. 
Epidemics have been more severe and the case fatality rates have been 
higher in small towns and rural districts than in the more dens ely populated 
cities. Even in cities the disease does not strike especially the crowded 
districts. In general, the incidence rates are lowest in large cities, higher in smaller towns, and highest in villages and rural districts. 
Age and Sex Distribution - Poliomyelitis is usually considered to he 
a disease of childhood. On the average about 65 per cent of the cases 
occur under the age of five years and 95 per cent occur under the age of 
ten years. The age incidence is likely to he higher in rural than in 
urban areas. 
This disease may occur at any age. During recent epidemics in New 
York and California the disease tended to attack the older age groups more 
frequently"than had been the case heretofore. 
About 55 per cent of the cases occur in males and per cent in 
females. This ratio has been quite constant at different age levels and 
in different sections of the country. 
Inculpation Period - It is difficult to determine the inculpation 
period in the human. Based on the occurrence of multiple cases in families, 
Aycock estimates that the inculpation period is from ten to eighteen days 
with an average of fourteen days. Epidemiological investigations should 
consider events taking place about two weeks prior to onset of the case in 
question. 
Modes of Transmission - It is assumed that poliomyelitis is spread 
by droplet infection from person to person, and the infective agent is 
discharged from the mouth and nose and enters the body through the same 
channel. It is considered that the virus is present regularly in the 
nasopharynx in the first days of Illness and disappears as the disease 
progresses. This would indicate that the period of greatest infectivlty is 
early in the disease. 
The prevalence of the infecting agent of poliomyelitis in any community 
during normal periods is not known, but during epidemics it is likely that 
a large number of the population harbor the virus for varying periods of 
time. Only a small number, however, of those individuals invaded by the 
virus actually develop symptoms of the disease. The temporary carriers are 
probably more important than the actual case in the spread of the disease. 
At the present time there is no practical method by which carriers may be 
detected. 
Falrbrother, Hurst and Jungblut have shown that the virus of polio- 
myelitis travels largely by way of neural pathways; namely, the olfactory 
nerve endings in the nasal mucous membrane. Once the virus has entered 
nervous tissue, its migration seems to continue along axonal pathways, 
passing from the olfactory tract through the hypothalamus, thalamus, and 
medulla to the spinal cord. 
Some workers have presented evidence that the disease may be trans- 
mitted through the gastro-intestinal tract. This has been done experimentally 
under increased Intestinal pressure or by direct contact with the mysenteric 
nerves. This condition is not likely to occur naturally. 
Though a few epidemics of poliomyelitis suggestive of milk-borne 
transmission have been reported by Aycock and others, it is not a common 
mode of spread of this disease. Due to the increase in prevalence during the summer months some workers 
have attempted to connect the transmission of poliomyelitis with an insect 
vector. It is doubtful whether poliomyelitis is spread hy this means. 
Direct or indirect contact with previous definite or suspicious cases 
can be traced only in 20 to 50 per cent of the cases Investigated. Recent 
reports from California and Tennessee indicate that it is possible to 
obtain evidence of contact in a larger per cent of instances than has 
heretofore been thought to be possible. 
Only exceptionally does poliomyelitis tend to spread within families. 
In the extensive epidemic in 1916 in New York only k,3 per cent of 8,651+ 
families attacked had more than one case. When multiple cases occur in a 
family, they usually come down together or within a short time of each 
other, signifying simultaneous infection from a common source. 
Incidence and Case Fatality Rate - Numerically, poliomyelitis is not 
a large problem in comparison with other infectious diseases. The sequelae, 
however, are disabling and crippling in from 25 to 60 per cent of the cases, 
and for that reason the general public tends to emphasize the problem. 
According to Leake, the mortality data available for the past three years 
indicate that poliomyelitis has accounted for about 800 death a year; 
epidemic meningitis, 1,200; tuberculous meningitis, 2,200; scarlet fever, 
2,500; dysentery, from 2,000 to 5,000; diphtheria, 5,000; typhoid fever, 
J+,500; pertussis, from to 7,500; syphilis, 11,000; tuberculosis, 
75,000; and automobile accidents, from 28,000 to 56,000. 
Based on house to house studies to determine the prevalence of diseases 
in an entire community, it has been estimated that for the greater part of 
the United States there are approximately ten paralytic cases per 100,000 
population. 
The mortality rate in the United States Registration Area varies from 
that when the incidence of poliomyelitis reaches one per 1,000 population 
than an epidemic is present. The Incidence in any community varies with 
the immunity in the existing population and the opportunity of spread of 
the infection. During the epidemic of 1916 in New York the incidence reached 
5 per 1,000 population. 
Poliomyelitis may be a malignant disease as regards fatality. The 
case fatality rate will vary markedly from year to year as evidenced by 
the fact that the rate varied from 50.7 to 5 per cent with an average of 
20.8 per cent in 20,568 cases recorded for 58 epidemics which occurred in 
various parts of the world from 189I+ to 1921, In New York City in 1916 
there were 8,928 cases and 2,407 deaths, a case fatality rate of 28 per 
cent. The case fatality rates for Tennessee for small numbers of cases 
for 195*+, 1955, and ten months of 1956 were 19-2 per cent; per cent; 
and 10.5 per cent respectively. 
The case fatality rate is likely to be low under the age of five years 
and increases as age advances. 
Immunity - An attack of poliomyelitis usually confers a permanent 
immunity. It has has been shown that neutralizing antibodies appear in the 
blood of humans convalescent from poliomyelitis and in monkeys recovered 
from experimental Infection. This can be demonstrated by means of the neutralization test by whiSh "blood serum containing antibodies when mixed 
with virus renders it non-infective for monkeys. A recent study has shown 
that only about 60 per cent of the sera examined from that particular group 
of convalescent individuals contained neutralizing antibodies even though 
each one had passed through an attack of the disease. 
It is thought that a barrier exists between the central nervous and 
the blood vascular systems and that the virus is usually confined to the 
nervous system. Harmon and Harkins state that the irregular outflow of the 
virus from the nervous system during the acute disease accounts for the 
variable appearance of neutralizing antibodies. 
A large percentage of individuals of all ages in the population who 
have had no obvious exposure to the disease carry neutralizing substances 
against the virus in the blood stream. The incidence of antibody Increases 
with age. The presence of the substances under these conditions has been 
interpreted as signifying an Immune state and has been produced in the blood 
as a result of specific contact with subinfective doses of the virus. The 
relationship between Immunity to poliomyelitis and the neutralizing sub- 
stances is not clear at the present time. 
Prevention and Control - The measures that have been applied in the 
control of poliomyelitis are on the whole unsatisfactory due to lack of 
definite knowledge of the etiology and mode of transmission. However, 
certain procedures may be Instituted which may be of value. 
Notification - All cases should be reported immediately to the health 
department. This should include the reporting of suspected cases as well 
as frank cases Recently the U. S Public Health Service has requested 
that cases of this disease be reported as "paralytic" or "non-paralytic". 
Isolation of Cases - All cases should be isolated for at least three 
weeks from date of onset. 
Disinfection -Concurrent disinfection of all discharges. The usual 
procedure should be applied to the disinfection of bedding, utensils, food 
remnants, etc. 
Quarantine - The usual procedure is to quarantine all children in the 
household for a period of three weeks. Under certain circumstances adults 
in contact with cases may also be quarantined. 
Prevention of the introduction of the disease from the outside in the 
case of children’s institutions by quarantine may be advisable. 
Voluntary "quarantine" of young children by parents may be advocated. 
Educational measures should he employed in an attempt to give the public 
accurate information concerning the disease and to keep the public Informed 
as to the progress of the epidemic. An attempt should be made to prevent 
the usual fear which is immediately aroused upon the appearance of the 
disease in the community. Cooperation should be encouraged in avoiding 
any unnecessary exposure of children in crowds, in travel and in visiting. 
Advice should be given as to keeping children well by avoiding undue or 
unnecessary fatigue, trauma and gastro-intestinal disturbances. Nothing 
is to be gained, as a rule, by closing schools. 
42 Diagnostic Facilities - Health department should he prepared to fur- 
nish diagnostic service and facilities through personnel thoroughly familiar 
with poliomyelitis. During ah epidemic it is only hy this means that early 
cases can he detected and the’ disease differentiated from numerous other 
acute conditions which may resemble poliomyelitis and he confused with it 
in the early stages. 
Vaccination - For the past two decades attempts have been made to 
produce an active immunizing agent against poliomyelitis hy means of attenuat- 
ing the virus hy means of chemicals, heat, desiccation and absorption to 
alumina gel. Following the use of these agents, neutralizing antibodies 
could he demonstrated in experimental animals. Following inoculation with 
the agents, some of the monkeys developed poliomyelitis after the intra- 
nasal or intracerebral application of virulent virus as a test of immunity. 
In view of the fact that the virus has difficulty in getting from the 
blood stream to the central nervous system, future experiments should 
explore the possibility of using the immunizing agent so that it will get 
through the blood vascular system and come in contact with the central 
nervous system. There appears to be an undetermined mechanism which 
prevents this process. 
Sprays - The normal mucous membrane and its secretions represent 
protective barriers against the invasion of pathogenic organisms. Any 
chemical substance or manipulation which may cause Irritation or trauma are 
likely to assist the entrance of infective agents. However, Armstrong and 
his associates recently have shown experimentally that a spray solution of 
picric acid and sodium aluminum sulphate would protect monkeys against the 
virus of poliomyelitis instilled into the nasal cavities, the solution 
forming a protective coating over the mucous membrane. The possibility 
of creating an artificial blockade by this means to prevent the entrance 
of the virus into the body is still an experimental procedure, but it is avail 
able for use by physicians at their discretion. No spray should be used 
unless advised by the physician. 
After Care and Rehabilitation - While it is not the duty of health 
officials to treat cases of poliomyelitis, they should be acquainted with 
the scientific procedures and be able to render any assistance and give 
advice in order that disability may be reduced to a minimum. Certain 
points such as placing the paralyzed extremities at rest in a normal 
position to prevent contractures, and the prevention of any undue mani- 
pulation or unnecessary treatment until the acute stage of the disease 
has subsided should be emphasized. The problem resolves Itself into one 
for the orthopedic specialist and the public should be Informed of the 
great benefit which may accrue if such a specialist is called in to super- 
vise the case before contractures and atrophy occur. Probably an orthopedist 
should see each paralytic case of the disease as soon as the diagnosis is 
made. 
Programs for the rehabilitation of crippled children are being con- 
ducted by many private organizations and by governmental agencies in a 
large part of the United States. If it became necessary to provide 
follow-up for a considerable number of poliomyelitis cases, the public 
should be informed about such services and the cases should be followed up 
so that these agencies can work efficiently. A nurse with special training 
in physiotherapy should be made available to the local health service for 
this purpose. TYPHOID FEVER 
Typhoid fever is an acute, specific, generalized infection, usually 
characterized by a gradual Increase in temperature, with or without diarrhea 
rose-colored eruption, slow pulse, and tenderness over the abdomen. 
The incubation period varies from seven to twenty-eight days; average 
ten to fourteen days. This bears an important relationship to the epidemio- 
logical studies. The average duration of the fever is about twenty-five 
days; case fatality is about ten per cent. 
Let us review just briefly some of the morphological and biological 
characters of the causative organism, B. typhosus, or Eberthella typhi as 
it is now known in recognition of its description in i860 by Eberth. It is 
a Gram negative, non-spore forming, motile rod. It is an aerobic, faculta- 
tive anaerobe; does not produce indol, and falls to ferment either lactose 
or saccharose. These latter factors are of importance in differentiating 
this organism from certain others of the enteric group. This organism is 
not difficult to cultivate on simple laboratory media, but does exhibit 
frequent morphological variations. The significance of these forms is 
not clear; there is no evidence that they are involution forms; it is 
probable that they represent phases in the life cycle. The type of variabi- 
lity with which we are concerned is the dissociative changes from "smooth’' 
to ''rough", and which we shall develop further in this paper. 
Typhoid bacilli does not thrive well outside the human body, but with 
favorable temperature, moisture, and food supply will live sufficiently 
long for indirect transmission, especially in water, milk, and certain 
other food supplies. 
The portal of entry is the mouth; excretion is through the feces and 
urine. The organism has been recovered from the sputum, and certain other 
body fluids. The gall-bladder, biliary passages, marrow, spleen, and 
mesenteric lymph nodes are the principal reservoirs of the human body. 
Typhoid fever Is transmitted hy direct and indirect contact. It may he 
spread directly from a person who has or has had the disease to one who is 
susceptible to it. It may be spread by indirect contact, in water, milk, 
milk products, oysters, vegetables, and other foods; also, by flies and 
fingers contaminated by human excreta. 
The mode of spread may be referred to as 
1. Water borne. 
2. Milk borne. 
3. Contact infections: 
a. Cases - acute, atypical, mild, or unrecognized. 
b. Carriers. 
c. Objects contaminated - utensils. 4. Other foods contaminated 
5. Fly borne 
Water borne: 
There is a seasonal variation. It may occur in the fall, winter, or 
spring, but usually in the late winter or the early spring. The outbreak 
is usually explosive, with gradual Increase of incidence until the peak 
is reached, and a gradual decline if the source of contamination has 
been removed.* There is a general distribution of cases throughout the 
area supplied by the polluted water - may be occasional outside cases. 
There is relatively a larger per cent of the cases among adults. Epidemics 
from this source are almost always preceded by premonitory diarrhea. It 
is usually possible to indict this source by a preliminary survey. The 
evidence may be confirmed by: 
A careful study of area with reference to source of contamination 
A bacteriological examination of the water may show colon bacilli 
A chemical analysis showing nitrites also indicates pollution. 
In suspected pollution of water, Immediate action should be taken to 
insure boiling of water for domestic purposes. 
Milk borne; 
Sources of the Infection include 
1. Delivery of milk to premises where a case exists 
2. A carrier employed on the dairy or farm producing milk sold in the 
community, raw or Imperfectly pasteurized. 
3. Washing utensils with polluted water; cleansing udders with con- 
taminated water. 
k. Milk may be contaminated by flies, or by dirt where there is 
improper protection. 
5. May be defective pasteurization. 
6. May be contaminated by the consumer. 
Milk is a favorable medium for the rapid multiplication of the 
organisms; therefore, massive doses may be Ingested. Immunity may break 
down, even in recently vaccinated individuals. 
Cases usually will be found along the route of a certain distributor. 
There is no seasonal variation as seen in the water-borne. The incubation 
period usually is shorter because of large doses of the organisms. A 
larger per cent of the cases occur among women and children. Often more 
than one case in a family occurs about the same time. More cases usually 
occur in families consuming considerable milk. The outbreak is usually 
sudden, with a rapid rise to the peak, and a corresponding decline. 
45 A thorough survey of the personnel, methods of distribution, and con- 
sumption should be made in order to determine the source. 
Contact infection: 
This may be the result of association with an acute case of the disease, 
a mild or unrecognized case, or with a carrier. The carrier problem in the 
transmission and control of typhoid fever has become one of great importance 
From two to four per cent of persona who have had the disease continue to 
discharge the organisms in the excreta. Every case, therefore, is a 
potential carrier. 
Outbreak due to carrier: 
Usually, isolated or sporadic cases occur. The number of cases is 
usually small, and Intervals between cases may be long. There is no 
seasonal variation. The outbreak due to a carrier is usually in an 
institution, or camp, where the carrier has to do with preparation or 
handling- of food. 
Fly-borne; 
The characteristics are similar to the carrier outbreak, except that 
fly transmission occurs more In the warm months of the year. This source 
is usually arrived at by elimination of other possibilities, as water and 
milk, plus insanitary conditions in the environment. 
In a review of the methods and mechanisms of artificial immunization 
against typhoid fever and its relation to the lowered incidence of this 
disease, it is well that we do not lose sight of many other factors which 
have abundantly contributed. In fact, it is considered by many that 
Improvement of water supplies, sewage disposal, and education of the public 
resulting in general knowledge of the transmission avenues, have been as 
Important as vaccination. 
It is proper to review briefly the history of typhoid vaccination, and 
to discuss certain factors which may influence the protective action of 
vaccines, that is, their efficiency as a prophylactic agent, and. some 
problems in the serological diagnosis which have arisen as a result of 
these vaccinations. 
The use of vaccines in the prevention of certain other diseases 
naturally suggested the use of such agents in typhoid. 
As early as 1888, Widal, and others, showed that animals could be 
protected against lethal doses of virulent typhoid bacilli by previous 
inoculation with killed typhoid organisms, allowing time, of course, for 
this immunity to be established. Next, it was found that the serum of 
these vaccinated animals contained specific anti-substances which were 
identical with those demonstrable in the serum of persons recently 
recovered from typhoid fever. Out of these observations was developed the 
possibility of human immunization. 
In 1896, Wright, in England, began to use killed typhoid suspensions 
in human inoculations. He observed that the procedure was safe, and was 
followed by demonstrable antibodies in the blood of vaccinated individuals. 
46 YEARS OF AGE 
DEATHS FROM TYPHOID IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-393 
KEY-EACH MAJOR GRID 
REPRESENTS 5 DEATHS The following year this same worker suggested the use of this vaccine 
in the armies of Great Britian. This was done, but these first efforts did 
not appear to have any appreciable effect on the incidence of typhoid. 
Following this apparent failure in mass Immunization, work was begun 
on better methods of preparation and standardization of vaccines. More 
suitable strains were selected, and methods of cultivation were improved. 
It is not Improbable that the phenomenon of dissociation was responsible 
for the early failures. 
In 1908, typhoid vaccination was introduced in the Army of the United 
States, using the English'M,Rawlins'T strain of typhoid bacilli. This strain 
had been selected for use in the British army because it produced in man a 
satisfactory titer of antibodies, and possessed what we now designate as 
smooth qualities. 
At first the Army vaccine consisted of a saline suspension of the 
organisms, killed at 53 degrees Centigrade for one hour, and standardized 
at 1000 million organisms per c.c. Actually, there were only about 500 
million per c.c. In 1917* 730 million each of para typhoid A and B were 
added. Reactions with this vaccine were considerable. In 1927* para-typhoid 
B was dropped, and typhoid Increased accurately to 750 million. It 
was now used in this state, giving three doses, each at weekly intervals. 
It is the practice at this time to give one-half c.c., followed by one c.c., 
doses at weekly intervals. 
In 1913, the Army had, In 80,000 men, only four cases of typhoid fever. 
From 1909 to there was only one death in the A.rmy from typhoid fever, 
while the civilian rate for the same period was 16.5 per 100,000; a sub- 
stantial reduction, however, from 35 in 1900. In 1900, typhoid fever was 
the fourth on the list as cause of death in the United States, hut in 1935* 
had reached twelfth place. During the World War (April, 1917, to November, 
1918) in men in the Armies of the United States, there were 
1329 cases of typhoid fever with 122 deaths. 
One attack of typhoid fever usually confers a life-time immunity. It 
is estimated that a second attack may occur in 2 to 3 par cent of cases. 
As we evaluate the immunity as produced by actual disease experience, and by 
vaccination, let us not lose sight of the fact that these individuals are 
from time to time subjected to sub-infective doses of organisms which 
doubtless aids in fortification of the immune mechanisms. 
Circulating antibodies usually disappear from the serum of recovered 
individuals in about seven months, and in the vaccinated person in a few weeks 
Immunity cannot, therefore, be explained on a basis of circulating antibodies. 
Then where are these substances? They must be in association with the cells 
of the body; rather, let us say, the cells of the retlculo-endothelial 
system. 
It is generally agreed that we cannot explain all immunity on a basis of 
antibodies. The cellular mechanism also plays an important part, to which 
we shall refer later. 
It is not our purpose to outline the technical features of the Widal 
test, but it is desired to point out some problems which have arisen in the 
serological diagnosis in the sometime vaccinated individual. It was 
47 difficult to determine whether antisubstances demonstrable in the serum, were 
due to infection with the organism, or to the effect of the vaccine, or 
previous experience with the disease. The problem is further complicated 
by what is termed "anamnestic reactions". These latter reactions are due to 
a return, or "recall’’, to the circulating blood of antibodies produced in 
response to a previously Introduced antigen under the stimulus of a subse- 
quent antigen. This second stimulus may not be the antigen which produced 
the existing antibodies. For example, an individual contracts Malta fever; 
he was vaccinated against typhoid fever six months ago; a Widal might now 
show a titer of agglutination which we would be inclined to accept as 
diagnostic. 
At this time let us mention some of the work which has been done in an 
effort to differentiate these agglutinations. We refer here to work with the 
H, or flagellar antigen, and the 0, or somatic antigen, and the Yi antibody. 
It was observed by Felix, in 192U, that vaccination produced almost 
exclusively the ’ H" type of agglutinins, while the infection produced 
chiefly the "O' type of agglutinins, and that we might differentiate these 
reactions by the use of the homologous antigen, observing the type of 
flocculation produced. 
We have already noted the fact of morphological variation in typhoid 
bacilli grown on artificial media. Arkwright has shown that the chief 
variants are: 
Smooth motile; smooth non-motile 
Rough motile; rough non-motile 
Antigenic changes, changes in pathogenicity and bio-chemical activities are 
results of these dissociations. 
Further studies by Felix have shown that there are smooth M0M strains 
which are inagglutinahle, and other which are agglutinahle in "0TT antiserum, 
also, that only these inagglutinahle virulent organisms produced sera which 
would agglutinate and protect. The inference is that the virulent organisms 
produce a third antigenic factor which he calls Vi. When the sera of 
animals immunized with virulent strains are prepared, or, as we would say, 
set up, with agglutinahle and inagglutinahle cultures, the agglutinahle 
strains take out both ”H" and "0" antibodies, hut not the Vi; on the other 
hand, Vi strains take out the Vi antibody, hut very little of the "H" and 
’’O'. The Vi antigen is present only in the living, non-heated organisms, 
is destroyed by 60 degrees Centigrade, and is only partially preserved by 
formalin. The conclusion is that vaccines should he prepared from VI 
antigen, since it is this fraction which is responsible for the production 
of protective antisuhstances, and gives us a more accurate differentiation 
of the vaccinated individual. 
Siler has worked with many of the strains which have been used in 
the preparation of vaccines at the Army Medical School. In protection 
tests he has found that vaccines prepared from avlrulent strains have failed 
to protect mice from infection when inoculated with virulent organisms. 
He has found, also, that virulent strains differ in their antigenic 
properties. He concludes that immunogenic property in typhoid bacilli is 
closely associated with virulence, and that heat killed, tricresol vaccines 
give better protection. 
48 Hawley and Simmons have studied the effectiveness of the Army and Navy 
vaccines in relation to dosage. They believe that the "Rawlins’1 strain is 
as efficient today as it ever was, and that decrease in efficiency can he 
explained on a basis of dosage. 
It is a well-established fact that there are many antigenic components 
in a bacterial cell, the principal ones being the protein and polysaccharide 
fractions; within these fractions there appears to oe a multiplicity of sub- 
fractions, as Indicated by Furth and Landsteiner working with the typhoid 
bacillus. 
The studies up to this time have suggested that among these various 
fractions of the bacterial cell, there is a specific, or essential, immuniz- 
ing antigen. 
Felton and Wakeman have made an investigation of the active 
Immunity producing properties, and some of the chemical characteristics 
of the fractionated typhoid bacillus. They have found that the killing 
temperatures and chemical preservation may alter the antigenic properties 
of a vaccine; that certain antlgenlcally inert substances, as lipoids, 
may actually inhibit the immunizing mechanism, and that certain growth 
nroducts of the organism in culture may do the same thing. In their 
preliminary report, it is indicated that an acetone extracted polysaccharide 
fraction is the essential immunizing agent. 
OUTLINE FOE THE CONTROL OF TYPHOID FEVER 
I. MEASURES OF IMMEDIATE IMPORTANCE 
A. Records 
1. Report cards in the hands of physicians. 
2. Epldemllogleal lnvestigation0 
a. Spot maps. 
h. Classification of findings. 
5. Tabulation of cases by days, weeks, months 
Tabulation of cases by age, sex, color. 
5- Tabulation of deaths by age, sex, color. 
B. Notification 
1. Compulsory reporting of cases 
C. Case findings on unreported cases. 
D. Investigation 
1. Investigation of cases as soon as possible. 
2. Complete epidemiological history on every case. 
3- Confirmation of diagnoses. 
E. Management of cases 
1. Isolation, screening. 
2. Hospitalization. 
49 3. Concurrent disinfection: 
a. Stools and urine. 
b. Bed linen and clothing. 
c. Utensils. 
d. Sputum and purulent discharge. 
e. Container with disinfecting solution for use of 
physician and attendant. 
f. No containers to be removed by milkmen. 
g. Frequent calls upon case. 
h. Terminal disinfection. 
i. Release cultures. 
F. Control of contacts. 
1. Vaccination regardless of history of typhoid. 
2. Examination of stools and urine if indicated. 
3- No member allowed to handle food until determined safe to 
do so, especially in food establishments. 
G. Control of carriers. 
1. Determination and registration of carriers. 
2. Check on known carriers twice yearly. 
3- Instruct carriers in hygiene. 
k. Prohibition of food handling by carriers. 
5. Efforts to eliminate carrier condition. 
II. MEASURES OF GENERAL IMPORTANCE 
A. Sanitation. 
1. Excreta disposal. 
a. Number of families connected sewer, privies, etc. 
b. Extension of sewer connections. 
c. Compulsory connection with sewerage system. 
d. Regulation of privy construction. 
e. Inspection. 
f. Treatment of sewage. 
2. Water supply. 
a. Frequent laboratory examination of water. 
b. Frequent inspection of plant and system. 
c. Filtration and chlorination. 
d. Swimming pools: Inspection, examination, chlorination 
3. Milk and dairy products. 
a. Inspection of dairies and examination of milk handlers 
h. Bacteriological examination of milk, 
c. Pasteurization. 
. Other foods: Shellfish and' vegetables 
5- Foods in general. 
a. Examination of food handlers. 
b. Inspection of food establishments. 
6. Fly control. 
a. Garbage disposal 
b. Screening. B. Vaccination. 
1. Establishment of clinics for vaccination. 
2. Vaccination of school children. 
C. Education. 
1. Responsibilities and dangers. 
a. Cause and how transmitted. 
h. Principal sources of Infection. 
c. Value of sanitation and vaccination. YEARS OF AGE 
DEATHS FROM DYSENTERY IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-355 
KEY -EACH MAJOR GRID 
REPRESENTS 10 DEATHS BACILLARY AND AMOEBIC DYSENTERY 
Dysentery is a symptom complex consisting of diarrhea with blood and 
mucous in the stools, usually associated with abdominal pain and tenesmus. 
The lesions are usually limited to the colon, appear as areas of ulceration, 
discreet in the amoebic type, with normal mucosa surrounding. In the bac- 
illary variety the mucosa between lesions tends to be hyperemic. 
Since ancient times dysentery has occurred sporadically, and in epidemics 
The epidemics have usually been associated with hot climates, filth, and 
general unsanitary conditions in the environment. In 1892, Councilman differ- 
entiated the pathology of the amoebic and bacillary dysenteries, and in 1898, 
Shiga proved the specific bacillus now known as the cause of the Shiga type 
of dysentery. 
With differentiation of the amoebic and bacillary types of dysentery, 
our knowledge of the transmission, and methods of control, much has been done 
to lower the incidence of these diseases. Epidemics still occur both in the 
tropics and in the temperate regions where proper sanitation is not observed. 
The dysentery bacilli belong to the large group of intestinal Gram nega- 
tive rods, differing from the typhoid and colon group in that they are non- 
motlle, and possess certain cultural and serological differences. 
There are two main groups of dysentery bacilli. One group Includes only 
the Shiga bacillus, is more virulent, possesses a neurotoxin as well as an 
enterotixin. The other group includes the Flexner, Hiss-Russell (Y), Sonne 
and other strains, all of which are less virulent than the Shiga, possess 
only an enterotoxln and ferment mannite in culture. Some mildly pathogenic 
strains usually produce only a mucous diarrhea without blood. The bacilli in 
man multiply in the small intestine. The toxins are absorbed, and act on 
special tissues. The neurotoxin produces paralysis in animals and stupor in 
man. The enterotoxln acts mainly upon the mucosa of the colon during its 
excretion from the blood, and causes a diphtheritic inflammation. In animals 
this can be produced by intravenous injection of the toxin, but not by inges- 
tion of cultures. In man the bacilli are found in the dysenteric stools, 
sometimes almost in pure culture in acute cases, and may persist in chronic 
ulcers producing the carrier state. Outside the body the organisms are 
easily destroyed, but may survive in water, milk, or moist soil three weeks 
if not exposed to sun. They will live two to five days in the intestines of 
flies. 
Incubation Period. 
Two to seven days. 
Period of communicability. 
Usually until diarrhea ceases. Actually until no more organisms are 
excreted in the feces. 
Incidence. 
All ages are susceptible, and no racial immunity is known. An exact 
estimate of incidence is difficult to obtain because many mild cases are not 
seen by physicians. High atmospheric temperatures favor spread of the organ- 
isms because of their survival outside the body and the presence of flies. 
Therefore, epidemics and sporadic cases are most common in summer and in tro- 
pical countries. Undoubtedly scores of small epidemics occur in this country every year, and many thousands of people suffer from the disease. The majority 
of cases of summer diarrhea in infants is caused by dysentery bacilli. 
Mortality. 
Severity of attacks depends mainly upon the variety of organism involved. 
The very young and the very old show the highest case fatality rates. In 
Shiga epidemics the mortality is often 30 per cent or more. In epidemics with 
the mannlte-fermenting group it is usually not over 5 per cent. 
Immunity. 
Agglutinins appear in the blood during convalescence and remain for one 
to two years. There is probably an immunity of uncertain duration against the 
strain of organism causing the disease, but not against other strains. During 
epidemics some people seem to develop agglutinins without a clinical attack. 
Sources and Modes of Infection. 
Man becomes Infected from water or milk, from food contaminated "by flies 
or human carriers, or hy direct contact with the discharges from active cases. 
Direct contact and flies are more important than in typhoid fever because of 
the enormous numbers of organisms present in the dysenteric stools. Monkeys 
are the only lower animals known to harbor the organisms. They sometimes 
suffer from acute bacillary dysentery. 
Carriers. 
Ordinarily the bacilli disappear from the stools within a week or two 
after cessation of symptoms, but about 3 per cerjt of cases become chronic, 
with localized ulcers which may harbor the bacilli for years. Shiga cases 
are more likely to become chronic. Relapses may occur. The chronic relap- 
sing case most often becomes a carrier. Chronic carriers may have no symptoms, 
and may excrete bacilli at Irregular intervals. They probably have small 
lesions in the colon. Two to five per cent of cases become carriers after 
an epidemic. Chronic cases and carriers are responsible for the persistence of 
the disease from year to year. They are dangerous as food-handlers and es- 
pecially if proper excreta disposal in not observed. Healthy carriers without 
a history of dysentery are rare. Some cases of chronic ulcerative colitis 
are really chronic bacillary dysentery. 
Epidemiology. 
In the middle ages there are said to have been very extensive epidemics, 
but in recent times they have been confined to smaller groups. In wars 
dysentery has been more dangerous than bullets. There were over 1,500,000 
cases in the federal army during the Civil War and 57,000 deaths. The longer 
troops are together the higher the morbidity rate and case fatality rate. 
There were serious epidemics during the World War. Prisons and asylums fre- 
quently have epidemics. Towns in unsanitated regions have epidemics, and 
contaminated city water supplies have given rise to them. Every year many 
epidemics occur in rural areas and villages in the Southern States. In the 
tropics epidemics usually coincide with the rainy season. The maximum inci- 
dence coincides with that of the housefly. 
Prevention. 
(l) In hospitals, institutions and camps great care must be taken to 
avoid spread of infection from active cases. (2) Attendants on cases should observe strict precautions 
(3) Fecal discharges of patients should be disinfected. 
(*0 Patients should not be discharged until stool culture is negative 
for dysentery bacilli on three successive examinations not less than 2k hours 
apart. 
(5) Chronic cases and carriers in camps and institutions should be 
isolated until free from dysentery bacilli. 
(6) Food-handlers in camps and institutions should be examined before 
employment. 
(7) All cases of diarrhea in camps, institutions, asylums or in communi- 
ties where sanitation is poor should be looked upon with suspicion. 
(8) Vaccination has a definite value in checking an actual outbreak of 
the disease and in reducing mortality but only lasts from two to three months. 
It has not been used extensively because other measures are usually sufficient 
and because of severe reactions following vaccination. Recently an "anavaccine 
from which the toxicity has been removed has been reported to give good results 
(9) Prevention of fly breeding and exclusion of flies from habitations 
and food, and especially from the dysenteric discharges of acute cases. 
(10) Early efficient treatment to avoid the carrier state. Amoebic Dysentery- 
End amoeba histolytica is the only pathogenic amoeba. It exists in 
two forms, trophozoite or motile form and cyst. The trophozoite measures 
10 to 30 micra in diameter, has hyaline pseudopods, moves rapidly at body 
temperature, and often contains red blood cells when found in a dysenteric 
stool. It soon dies after leaving the body. The cyst measures 6 to 15 
micra in diameter, when mature has four nuclei of characteristic structure 
and is resistant to low temperature if kept in a moist condition. It is 
quickly killed by drying. It will survive two days in the Intestines of 
a fly, and a month or more in clean water. Infection takes place only 
by the ingestion of cysts. Reaching the cecum these excyst and under 
proper conditions, which are poorly understood, invade the intestinal wall 
and produce ulcers. Symptoms are dependent upon the extent of ulceration, 
which may occur anywhere in the large intestine and rarely in the ileum. 
It is probable that different strains of E. histolytica vary greatly in 
their Invasive power and therefore in the frequency with which they produce 
symptoms. 
Incidence 
Amoeblasls, that is, the presence of E. histolytica in the stools, 
is widespread throughout the world. About 7 to 10 per cent of people are 
infected in temperate zones, 20 to 80 per cent in the tropics. The 
incidence is to 50 per cent in some isolated communities in the 
Southern States. In unsanitated areas the incidence of amoebic infection 
is rapidly built up during childhood and is maintained at a fairly con- 
stant level throughout the adult decades. Acute amoebic dysentery is 
commonest in young and middle-aged adults but may occur at any age. The 
sexes are equally affected. All races are susceptible, but persons going 
to an area where much amoebic dysentery occurs seem to be especially 
susceptible. Most of those harboring the parasite are apparently healthy, 
even though they are infected with a strain of amoeba which is highly 
pathogenic. Acute amoebic dysentery may occur anywhere but is much more 
common in the tropics than in temperate zones and in the summer than in 
the winter. The factors responsible for this are not known, but they are 
probably related to the condition of the host, to food or to bacterial 
infections of the intestinal tract. Secondary bacterial infection may be 
Important in producing extensive ulceration. 
Incubation Period. 
Seven to one hundred days, and some Infected persons never develop 
clinical symptoms. 
Period of Communicability. 
As long as cysts are excreted in the stools, which may be a lifetime. 
Sources and Modes of Infection. 
Infected food-handlers, polluted water supplies, infected feces 
exposed to flies, or human fecal material used as fertilizer in gardens. 
Food-handlers and flies are common sources of Infection; polluted water 
may be a source of infection from wells, springs, or streams, or from cross 
connections between sewers and pure water supplies in cities. Milk is 
rarely if ever a source of Infection. The slow multiplication of the organisms, their relatively small number, the slow development of the 
disease and the absence of spread from one acute case to another make 
amoebic dysentery more sporadic and less epidemic than bacillary dysentery. 
Reservoir animal hosts of E. histolytica are a possible source of human 
infection but this is undoubtedly rare. Monkeys, dogs, cats, and rats 
have been suffering from acute amoebic dysentery. Hogs sometimes harbor 
E. histolytica without symptoms. It is not known whether these strains 
would produce lesions in man. 
Epidemiology. 
Epidemics of acute amoebic dysentery of small and large proportions 
have been reported. The source of Infection and the mode of transmission 
determine the epidemic picture which is produced. In India a multitude 
of polluted wells causes a highly endemic condition in which acute cases 
occur constantly. In the Philippines soldiers on the march drank water 
from polluted streams, producing an epidemic. On the Mexican border an 
epidemic among troops seemed to have been produced by flies carrying 
infected fecal material from insanitary privies to food. The same con- 
dition seemed to cause a slow spread of the infection through a rural 
community in Tennessee. In Chicago pollution of constantly recirculated 
water in a hotel by a sewer connection produced an epidemic in which the 
transient guests scattered to all parts of the country before their 
clinical symptoms developed, A food-handler may infect: 
(l) a whole family 
(2) many persons in an institution, or 
(3) occasional guests at a hotel. 
The long incubation period and the irregularity of symptoms often clouds 
the epidemic picture and hides the source of infection. 
Immunology. 
Complement-fixing antibodies are present in most Infected persons. 
An acute infection is usually f ollowed by a latent period of partial cure, 
which suggests local or partial or temporary immunity, but the frequency 
of recurrences suggests that a general immunity 1s not developed. Monkeys 
have been reinfected after cure. Spontaneous permanent disappearance of 
the infection without treatment has not been reported in man, but has 
occurred in certain animals which are not very suitable hosts, such as 
dogs and rats; and, with certain mild strains of E. histolytica has occurred 
in kittens which regularly die from highly pathogenic strains. 
Prevention. 
The acute case does not usually pass cysts but may do so. Although 
he is not usually a source of infection, his excreta and bed linen should 
be sterilized and attendants should observe proper precautions. The cyst 
carrier is the only source of transmission. It would be ideal if all 
public food-handlers could be examined to detect carriers, but under 
ordinary conditions this is not feasible. Frequent skillful examination 
would be necessary to make it effective. All detected carriers should be 
treated regardless of whether they have ever had symptoms. Cases and 
carriers should be warned that one course of treatment usually does not 
cure and should be followed at intervals for one year to be sure of a cure. Vegetables should not be eaten raw In regions where human excreta are used 
for fertilizer. Sanitary disposal of feces and their protection from 
flies is most important. Fly-breeding should be eliminated and flies 
excluded from houses and food. Private and public water supplies should 
be protected from pollution, and city health authorities should see to it 
that cross-connections are not allowed to exist between sewer pipes and 
pure water supplies. 
Diagnosls of Type of Dysenter 
Clinical Course. 
Bacillary dysentery is usually more acute than amoebic, with higher 
temperature, more prostration, and toxemia, and shorter in duration. 
Gross Appearance of Stools. 
Bacillary stools have a pink, purulent appearance, blood and pus 
intimately mixed, and mucus friable. Amoebic stools are more watery, with 
relatively little pus; blood and mucus are not so intimately mixed and 
mucus is more tenacious. 
Microscopic Appearance of Stools. 
Bacillary stools contain many polymorphonuclear leucocytes and many 
large mononuclears, both types usually showing degeneration. Amoebic 
stools have fewer polymorphonuclears, red blood cells are more in masses, 
and motile amoebae are usually present. Neither the gross nor the micro- 
scopic appearance, however, is absolutely reliable if amoebae are not found. 
Stool Cultures. 
In the absence of amoebae, cultures should always be made. Amoebae may 
appear on culture in suitable media when not found microscopically. 
Culture should be made for dysentery bacilli. Special technique is 
required to isolate either amoebae or dysentery bacilli, and directions 
should be followed carefully. Suitable fresh specimens, proper treatment 
of material, and proper media are essential. Routine cultures for dysentery 
bacilli often fail for lack of these precautions. 
In chronic dysentery proctoscopic examinations and examination of 
scrapings from ulcers both microscopically and culturally are often 
Important. Sometimes repeated examinations are necessary. Some cases 
show both amoebae and dysentery bacilli. LIFE STAGES and DEVELOPMENT OF THE MOSQUITO 
ANOPHELES 
MALARIA-CARRYING MOSQUITO 
CULEX 
PEST OR COMMON MOSQUITO 
EGG 
A FEMALE MOSQUITO AFTER 
SUCKING A BLOOD MEAL. LAYS 
HER EGGS ON WATER SURFACE. 
— ANOPHELES MOSQUITO EGGS 
ARE NOT HELD TOGETHER BUT 
EACH HAS A SEPARATE FLOAT. 
CULEX — 
OR COMMON MOSQUITO EGGS 
ARE HELD TOGETHER IN RAFTS 
TEMPERATURE OF WATER 
AND SEASON OF YEAR IN- 
FLUENCE THE HATCHING TIME- 
USUALLY 6 HOURS TO 3 DAYS. 
DETAIL OF 
EGG. 
DETAIL OF EGG. 
GROUP OF 
ANOPHELES EGGS. 
EGG RAFT. 
LARVAE 
Mosquito larvae or wiggle- 
tails ARE HATCHED FROM 
MOSQUITO EGGS. 
LARVAE ARE CLASSIFIED AS 
TO SIZE AS FOLLOWS: 
I. THOSE JUST HATCHED; 
Z ONE QUARTER SIZE; 3. ONE 
HALF SIZE; 4. THREE QUART- 
ER SIZE; 5. FULL GROWN 
LARVAE. 
—ANOPHELES LARVAE LIE 
PARALLEL TO WATER SURFACE. 
CULEX »- 
OR COMMON MOSQUITO LARVAE 
LIE AT AN ANGLE TO WATER 
SURFACE. 
TEMPERATURE OF WATER, 
SEASON OF YEAR, AND THE 
FOOD SUPPLY GOVERN LARVAE 
GROWTH TIME WHICH VARIES 
FROM 7 TO 90 DAYS. 
PUPAE 
Mosquito pupae or tumblers 
DEVELOP FROM LARVAE, 
— ANOPHELES PUPAE HAVE 
WIDE BREATHING TUBES AND 
LONG HEADS. 
CULEX ► 
OR COMMON MOSQUITO PUPAE 
HAVE LONG NARROW BREATHING 
TUBES AND ROUND HEADS. 
DURATION OF PUPAE STAGE, 
I TO 3 DAYS. 
ADULT 
The ADULT MOSQUITO DEVEL- 
OPS FROM THE PUPAE. 
—ANOPHELES MOSQUITOES 
REST WITH THEIR BODIES AT 
AN ANGLE AND SOMETIMES 
PERPENDICULAR TO SURFACE, 
CULEX ► 
OR COMMON MOSQUITOES REST 
WITH THEIR BODIES PARALLEL 
TO SURFACE. YEARS OF AGE 
DEATHS FROM MALARIA IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS-235 
KEY- EACH MAJOR GRID 
REPRESENTS 2 DEATHS MALARIA 
The history of malaria in Texas dates hack to its earliest settlers. 
The vastness of malaria throughout the world, particularly in the tropical, 
semi tropical and temperate climates (of which Texas is in the latter two) 
makes it very difficult to incriminate any particular race of people or 
even the approximate century that the malarias may have been introduced in 
Texas. At this writing we do know that malaria is one among the five (5) 
leading communicable diseases in the Eastern and Southern sections of this 
state. The chart showing the deaths from malaria by age groups for the year 
1938 indicates equally as much as any words can the wide range of fatal cases. 
While the chart shows the ages of only two-hundred nineteen (219) of the two 
hundred fifty-six (256) death certificates issued caused by malaria in Texas 
during 1938, the remaining thirty-seven were over eighty and under ninety- 
nine (80 to 99) years. This is very significant in that it shows deaths can 
and do occur from malaria in all age groups from birth to the age of ninety- 
nine (99) years. The mortality of malaria is estimated conservatively at 
one death to represent approximately each three hundred (300) active, acute 
cases of the disease. Since comparing the data available we find the year 
1938 has the lowest death rate from malaria in Texas of any of the previous 
yearly records. We may assume from these data that approximately seventy 
thousand five hundred (70,500) cases of malaria occurred in Texas during 1938. 
These figures would indicate that approximately two per cent (2$ of the in- 
habitants in the established malaria areas were afflicted with malaria during 
1938. This is a very conservative estimate of the prevalence of malaria for 
the reason that many cases of malaria are very mild knd are treated with home 
remedies and not seen by the family physicians, and therefore are not counted 
or even estimated in the tabulations on this chart. It is,V however, the con- 
sensus of opinion among both the medical profession and laity alike that 
malaria is an impoverishing disease and it is an unnecessary disease. Malaria 
can be prevented; it can be controlled; it can be eradicated if enough con- 
certed effort is exerted by a community. 
The synonyms of malaria are (a) chills and fever; (b) swamp fever; 
(c) ague; (d) intermittent fever; (e) every other day or every third day fever. 
There are three separate malaria fevers as we know them today in the United 
States, and all three of the malaria fevers occur in Texas. They are Tertian 
malaria fever, Estlvo-Autumnal malaria fever, and Quartan malaria fever. They 
each have their own individual causative organisms, and they do not mix or 
fight each other. It is not uncommon for a person to have two of these malaria 
fevers at one time, and in a few rare Instances, all three malaria fever organ- 
isms have been found in a human in the same drop of blood collected for diag- 
nostic examination. 
The causative agents for all malaria fevers are the respective Tertian, 
Quartan, and Falciparum malaria plasmodia. Malaria plasmodia are animals that 
live, thrive, and reproduce in the red blood cells of man and in the bodies and 
salivary glands of female Anopheline mosquitoes. The only natural way man can 
become Infected with malaria is through the bite of an infected Anopheline mos- 
quito. And the only way a female Anopheline mosquito can become infected with 
malaria plasmodia is by biting a human that has adult malaria plasmodia in his 
circulating blood. 
The parasitology of all three of the malarias is well defined and is a 
standard part of the laboratory work. The blood changes are the same in all 
three types of malaria, however, the toxicity differs in individuals as well 
as in each type of malaria: (1) The penetration of red blood corpuscles by the animal parasites. 
(2) Multiplication of the parasites and the concomitant destruction 
of the red cells in which they develop. 
(3) Liberation of pigment into the blood plasma. 
(4) The presence of free parasites and parasitized blood cells so 
altered as to act as foreign bodies in the circulation. 
(5) A slight increase in white blood cells, chiefly phagocytes, as 
the macrophages, polynuclear and transitional forms of cells. 
(6) The occurrence of melanemia, clumps and granules of melanin taken 
up by the white blood corpuscles, easily seen in stained speci- 
mens . 
The entomology relative to all three types of malaria is the same, i.e., 
the same species of mosquito may carry any one of the three species of malaria 
plasmodia, while only the genus Anopheles (mosquitoes) have been found to be 
able to transmit malaria plasmodia to man. In the United States nine species 
of this genus (Anopheles) have been proven to be capable of successfully 
transmitting the disease either in the laboratory or in nature, or both. They 
are as follows: 
(1) A. quadrimaculatus (^) 
(2) A. punctipennis (5) 
(5) A. pseudopuncitipennls (6) 
A. crucians (7) A. atropos 
A. albimanus (8) A. barber! 
A. maculipennis (9) A. walker! 
For more detailed information about mosquitoes see article :,Life and 
Habits of Mosquitoes", a regular Texas State Department of Health publication. 
The epidemiology of malaria consists of the following: 
a. Reported information of suspected cases of malaria and 
community investigations of factors involved. 
b. Diagnosis completed only by laboratory confirmation. 
c. To determine, if possible, whether or not the case is acute 
or relapse from a sub-acute stage or a chronic case of malaria. 
d. Investigate and give study to possible sources of infection, 
such as contact with some other community within the last 
two or three weeks or with other cases of malaria in com- 
munity. 
Study the mosquito population in community where case or cases 
are present. 
Study the housing and anti-mosquito measures in use by persons 
known to have been sick recently. 
e. Complete laboratory examination of blood specimen of the suspected 
malaria patient. 
f. The catching of an adequate supply of mosquitoes for identifica- 
cation and possible dissection purposes. 
g. A compilation of data and a report of situation to proper 
authorities. 
The diagnosis of malaria in cases where a laboratory is not available 
sometimes is quite difficult due to the fact that several diseases have 
similar physical signs in their incipiency. In a differential diagnosis of 
malaria by physical signs only, always consider the possibility of encounter- 
ing one of the following diseases: 
a. Dengue fever 
b. Influenza 
c. Heptatic abscess 
62 d. Typhoid and possibly paratyphoid fever 
e. Undulant fever 
f. Tularemia 
g. Early tuberculosis 
h. Acute rheumatic fever 
i. Septicemia 
The pathology of malaria may be very simple and of short duration, or 
it may be serious and produce fatal results to the patient. The sequelae 
of malaria depends considerably more upon whether or not complications 
develop than upon the type of the malaria the patient is afflicted with. 
The clinical portal of toxic or complicated malaria may be defined 
according to the pathological signs and physical exacerbations, as 
1. Algid type 
2. Pneumonic or congestive type 
5. Bilious type 
J+. Comatose type 
5- Choleraic and dysenteric types 
6. Hemorrhagic or "black water fever 
Of greatest public health importance is, of course, the prevention of 
the spread of the disease. Second in importance is the assistance that can 
be given the community to prevent malaria carriers from Infecting Anopheline 
mosquitoes, thereby endangering the community with the disease. It is highly 
Important that all cases of malaria be treated by the family physician; that 
proper screening is done to prohibit mosquitoes from transmitting the disease; 
that mosquito eradication is conducted where practical and economical. When 
laboratory work is done modern malaria microscopy should be stressed, as well 
as thorough treatment to prevent the development of malaria carriers. When 
in doubt the City or County Health Officer should be consulted. 
The first requisite in the prevention of malaria in any community is 
leadership by energetic, qualified public health officials - doctors, nurses, 
public health sanitary engineers and sanitarians. 
The next step to be taken is the establishment of a local community 
plan which everybody may participate in. The plan should be broad enough to 
develop the malaria prevention problem along several lines, as persons possess- 
ing different qualities may unselfishly spend their talents for the common 
good of the community --we find listed in the order of importance: 
1. Proper advice by the family physician is the most profitable in 
vestment. 
2. Employment of known measures for destroying larvae of anophelines 
and the eradication of breeding places of such mosquitoes. 
3. Blood examination of persons living in infected centers to determine 
the incidence of Infection. The Individual with malaria parasites in his blood 
should be protected from bites of mosquitoes. 
4. Screening sleeping and living quarters; use of mosquito nets 
3. Killing mosquitoes in living quarters. 
6. Education of the public as to the mode of spread and methods of pre 
vention of malaria. TICK-BORNE DISEASES OF THE SOUTHWEST 
The principal diseases transmitted to man by ticks in the Southwest 
are Relapsing Fever, Tularemia, and Rocky Mountain Spotted Fever, 
Relapsing Fever 
The period of incubation of Relapsing Fever is from two to twelve 
days, usually five to eight. There may he a prodromal stage of from a 
few hours to two or three days consisting of headache, loss of appetite, 
and lassitude. 
The onset of this fever is acute with chills, aching of the head, 
hack, and Joints, nauseau and vomiting. The temperature rises from 98 F. 
to 105o-104° F. and is accompanied with an increase in pulse and respira- 
tion. The temperature remains high from five to six days, often with 
fluctuations of three to four degrees centigrade. During this period 
there is nausea and vomiting, dry and hot skin, light perspiration, and 
Jaundice. Constipation may ensue, hut diarrhea, nose bleeding, and 
hemorrhages from the intestinal tract, gums, and ears are most often 
observed. Delirium may he present?hut rarely stupor. Enlargement of the 
spleen and also albuminuria with rapidly developing anemia is common. 
Moderate granulocytic leucocytesis is present, and the spirochetes may 
he demonstrable among the granulocytes. 
About the sixth or seventh day the patient apparently returns,to nor- 
mal. Within six or seven days after the afebrile state relapse again 
ensues. The symptoms of this second relapse are the same as those of the 
first, hut they only last from three to four days, ending with crisis. 
A third and fourth relapse may occur; very rarely more than four relapses 
take place. Clinically it is difficult to differentiate between Relapsing' 
Fever, Malaria, Dengue, Smallpox, Influenza, Yellow Fever, and the early 
stages of Plague. Weil's disease may also simulate this picture. 
The following procedures are used in the laboratory diagnosis of 
Relapsing Fever; 
(l) Demonstration of the presence of spirochetes in the blood during 
relapse affords a positive diagnosis of this fever. The spirochetes may 
be examined by direct wet smear under a cover glass, either by bright or 
dark field Illumination, or a thick or thin smear may be stained with Giemsa's 
or Wright's stain. 
(2) Blood from the infected individual may be injected intraperitonlally 
in a white rat or mouse. Within four to six days spirochetes can be 
demonstrated in the blood of the mouse. They are not numerous in the 
peripheral blood, during the first few days of the disease. 
The prevention of relapsing fever is very simple; The separation 
of man from the vector by the isolation of all convalescents and the 
protection of all persons from such vectors as lice and ticks. 
Tularemia 
Tularemia is an infectious disease produced by Bacterium Tularense. 
The etiological agent is present in Infected rodents, especially rabbits. 
It is secondarily a disease of man, being transmitted from the animal 
reservoir to man by the bite of ticks, deer flies, or by handling the 
dead bodies of infected rodents. The incubation period of this disease 
is from one to ten days. The average period is three and one-half days. The onset is very sudden and is characterized by chills, headache, 
vomiting, aching bodily pains, sweating, fever, and prostration. This 
disease manifests Itself in four definite clinical types which are the 
Ulcero-Glandular, Oculo-Glandular, Glandular, and the Typhoid type. A 
pulmonary type might well he included. 
Within forty-eight hours after the onset of the Ulcero-G-landular type, 
the patient complains of pains in the area of the lymph glands which drain' 
the site of infection. These glandular pains are accompanied hy swelling 
of the glands involved, which are only those of the immediate vicinity of 
the site of infection. These glandular pains are preceded hy a papule 
at the site of the insect hite, which breaks down and leaves a ragged ulcer 
This primary site is often found on the back of a finger. 
The skin area over the infected glands is reddened. The glands 
often break down and discharge purulent material. Incision of fluctuant 
glands is usually ill advised, as it results in chronic sinuses which 
prolong the course of the illness. 
In about half the cases these glands do not break down, but remain 
hard, palpable, and rather tender for two or three months, gradually 
returning to normal. The lymph glands other than regional are usually 
only slightly involved. 
Subcutaneous nodules, varying in size from that of a pea to one 
centimeter in diameter and numbering from two to thirty are sometimes 
present on the anterior aspect of the forearm and hand. The nodules are 
found along the blood vessels from the ulcer on the finger to the axillary 
glands. 
Loss of weight, extreme weakness, recurring chills, sweating, and 
prostration are characteristic of the active stage which lasts from two to 
three weeks. 
In general, the Ocula-Glandular type presents the same symptoms as 
the above mentioned type, except that the primary lesion is in the 
conjunctival sack instead of the skin. 
The papules usually occur on the lower lid. The eye manifests 
irritation, redness, and lacrimatlon. The preauricular, parotid, 
submaxilliary, anterior cervical, and, in severe cases, the axilllary 
glands, are infected. 
The glandular type is characterized by the absence of a primary 
lesion at the site of infection, also by the marked swelling of the 
regional lymph nodes. This type resembles the Ulcero-Glandular. 
The Typhoid type of Tularemia is chiefly characterized by the 
absence of a primary lesion and the swelling of the lymph nodes. The 
general symptoms of this type resemble those of Typhoid Fever. The onset 
and duration of this type is the same as that of the Oculo-Glandular type. 
Fever is always present in all four types of Tularemia. Patients 
show constantly an Initial rise in temperature, remission, and secondary 
rise. Following the initial rise there is a remission of one, two, or 
three days which is followed by a rise to the original height. After 
this there is a gradual decline to normal which may take two or three 
weeks to gain. Convalescence of Tularemia is very slow, and patients in this stage 
are often unable to work after six months or even a year. This weakness 
is very characteristic of Tularemia. 
Relapses of fever lasting six to eight days have occurred as late as 
ten months after the patient had apparently recovered. 
The clinical diagnosis of Tularemia is easily made, providing the 
physician will keep in mind the following points: 
(l) A history of the patient having dressed a wild rabbit or being 
bitten by a tick. 
(2) A primary lesion of the skin in the form of a papule developing 
into an ulcer. 
(5) Persistent glandular enlargement in the regions draining the 
primary lesion. 
(J+) A fever of from two to three weeks' duration and of an undulating 
nature. These things should be kept in mind to prevent the clinician 
from calling it ’’flu", septic infection, typhoid fever, or pneumonia; 
the aerologists from calling it undulant fever on account of the cross- 
agglutination with melitensis and abortus, or typhus because of a high titre 
in the Weil-Fellx reaction; the pathologist from calling it tuberculosis 
because of the lesions produced in the lymph glands, and the dermatologists 
from calling it sportrlchosis due to the subcutaneous nodules. 
The bacteriological diagnosis of Tularemia is made to verify the 
clinical diagnosis after the physician has recognized one of the above 
four points in his patient. .The procedure may be one or both of the 
following methods: 
(l) By obtaining an agglutination of Bacterium Tularense with blood 
serum taken from the patient not earlier than the second week of illness 
and noting an increase in the agglutination titre of the serum taken a 
few days later or on the third week of the disease. 
(2) By isolation of Pasteurella tularensis from guinea pigs inoculated 
with material from the primary lesion, or from the enlarged glands or' 
the blood of the patient. Microscopic examination of the cover-glass prepara 
tions taken direct from the patient is useless. After subcutaneous 
inoculation of the guinea pig, death occurs in five to eight days; 
at pos.t-mortem there is a whitish membrane-like area at the site of 
inoculation. There is a bubo, generally in the cervical axilliary, or 
Inguinal region, containing dry, yellowish caseous material; the spleen 
is greatly enlarged, very dark in color and contains yellowish white 
discrete, caseous granules up to one M.M. in diameter, projecting slight- 
ly above the surface; there are numerous granules in the liver; the 
lungs are rarely Involved. The organisms are present in enormous num- 
bers in the spleen, in smaller numbers in the liver, bubo, and heart's 
blood. 
The prevention of Tularemia is carried out in the following ways: 
(l) Cooking thoroughly any wild animal used for food, especially 
rabbits. (2) The use of rubber gloves when working In laboratories where 
necropsy on infected animals la being performed. 
(3) The use of rubber gloves by cocks, hunters, and market men in 
dressing rabbits. 
{k) Use of an Immune person for dressing rabbits where possible 
(5) Freezing the rabbits for thirty days or longer. 
(6) The use of the ordinary disinfectants. 
The only treatment for Tularemia is symptomatic. Complete rest in 
bed is probably the best single measure. Excision or even incision of 
the glands is not advised. No drug, preventive vaccine, or serum has 
been found yet. 
Rocky Mountain Spotted Fever 
Rocky Mountain Spotted Fever is an acute, endemic, febrile disease 
which is transmitted accidentally to human beings by the bite of an infec- 
tive wood tick, Dermacentor andersonl. 
The prodromal and early symptoms of Rocky Mountain Spotted Fever 
resembles closely those of the other acute, eruptive, febrile diseases 
and, as in those, vary in degree; therefore, it is difficult to estab- 
lish an early diagnosis in the disease. During the progress of this 
disease the following symptoms appear; a short prodromal period 
lasting two or three days during which the patient has a general malaise 
and chilly sensation. This is frequently followed by distinct chills, 
pronounced headache, and muscular pains. Rash and rose colored eruption 
are seen early. This rash and rose colored eruption occurs on the face, 
neck, and upper thorax. From twenty-four to forty-eight hours later 
in the wrist, forehand, ankle, and lumbar region of the back appears 
the characteristic petechial eruption, which is rose-red in color, 
changing rapidly to dark bluish-red. This is the result of hemorrhages 
from small blood vessels and will not disappear on pressure. The 
petechial increase in size, become purpuric and are accompanied by 
sloughs on the dependent parts of the body in the more severe cases. 
Not infrequently sloughing of the soft palate and scrotum appears in 
the human. The tongue has a yellowish white coat and the cojunctlva 
shows a yellow tinge in the later stages of the disease. Delirium is 
rare, the mind usually being clear. Extreme lassitude is the rule, 
constipation and albuminuria are common. The temperature is high from 
seven to ten days in uncomplicated cases, while in complicated cases it 
may be prolonged. The respiration and pulse are rapid, with the latter 
out of proportion to the degree of temperature, due to the toxemia. Con- 
valescence is slow but complete, with the temperature dropping rapidly. 
The clinical diagnosis of Rocky Mountain Spotted Fever is made from 
the history and surroundings of the case and the character of the erup- 
tions. It is usually easily arrived at after the petechial eruption has 
appeared, except in rare cases where the history doesn't exclude possibility 
of typhus fever infection. In such cases, blood inoculation into guinea 
pigs will easily establish the diagnosis because these two diseases are 
distinguishable in this animal both by character of lesions and by 
absence of cross immunization. The history of the tick bite is usually 
found to be from three to twelve days previous to the onset of the sickness. When there is no history of a tick bite and the tick has 
dropped off, the site of the bite is hard to locate. This is the habit 
of the tick Dermacenter andersoni. In some cases slightly elevated rose 
colored and macular eruptions appear on the face, neck, hands, and 
upper thorax before the characteristic petechial eruption is visible. 
These cases may easily be mistaken for measles or early smallpox or other 
exanthematous febrile diseases. 
If a careful examination is made, the primary eruptions of Rocky 
Mountain Spotted Fever will not be confused with early appearing erythemia 
or the diffused red-blush of scarlet fever, or with the rapidly changing 
papules and vesicles of chicken pox, or with the localized abdominal 
rose spots of typhoid fever. From the standpoint of subjective symptoma- 
tology, especially as regards headache and myalgia, only typhus and 
smallpox are likely to be comfused with Rocky Mountain Spotted Fever. 
In the biological diagnosis of Rocky Mountain Spotted Fever, a blood 
Inoculation from the infected individual is made intraperitonially 
into a male guinea pig. This brings about swelling of the scrotum and 
inguinal region of the animal and hemorrhages of the brain which produce 
death in the animal, in the case of Rocky Mountain Spotted Fever. In 
the case of Typhus, swelling of the scrotum and inguinal region takes 
place but the animal never dies, thus differentiating between the 
two diseases. Agglutination tests using non-specific antigen, proteus 
OX-19 and CX--K, is also used in diagnosing this disease. The same 
diagnostic test is used in typhus fever. An early high titre with 
Immediate and rapid increase is diagnostic of typhus and differen- 
tiates it from Rocky Mountain Spotted Fever, which Infrequently has this 
early high titre and rapid increase. 
There are three measures which we, as individuals, may use to 
prevent spotted fever: 
(l) Avoid ticks. 
(2) Remove ticks from the person as early as possible 
(5) Be vaccinated. 
On camping trips, if it is necessary to sleep in the open, care should 
he used in selecting a site for placing the hed, as ticks will crawl 
into a hed laid on the ground. Since ticks are usually most numerous 
where rodents are most abundant, areas well populated with rodents should 
he avoided. The safest camping ground is undoubtedly in standing timber 
where low vegetation is scanty. Proximity to trails and old roads should 
he avoided. In sage-brush sections, avoid the sage-brush. Avoid 
brushy areas along streams as camping grounds. The dog tick is far more 
likely to be present along the course of streams than is the wood tick. 
Persons should be especially watchful when walking along trails. Ticks 
tend to concentrate on vegetation along the sides of trails and in the 
bushes along the edge of wooded areas. Similarly, vegetation along road- 
sides and grassy strips in the middle of little used roads are often very 
dangerous. It is especially desirable to watch the clothing when 
following trails or old roads. 
In the prevention of tick bite, the first precaution is the wearing 
of such clothing as will prevent ticks from getting underneath. This 
may be accomplished to a considerable extent by wearing high boots, 
leggings, puttees, or socks that are worn outside the trousers legs. With such precautions taken, most ticks will crawl up the outside of the 
clothing and can he removed from the neck when contact with the skin 
makes their presence known. Passing the hand over the neck occasionally 
to feel for ticks is a good habit to acquire. 
Ticks are far more likely to secure a hold on rough clothing than 
on clothing of smoother texture. There are advantages in both, however. 
Fewer ticks secure a hold on smooth clothing; but, on the other hand, 
on cloth with a heavy nap their movements are impeded and are necessarily 
much slower. If the legs of the trousers are carefully watched, most 
ticks can be picked off soon after they catch hold. 
In spite of precautions, however, a certain number of ticks will 
reach the body through the various openings in the clothing. It is 
therefore important that the above precautions be supplemented by the 
examination of the inside of the clothing and of the body. Since 
ticks seldom attach immediately (unless late in the season), and 
are seldom infectious until after having been attached for a few hours, 
such examinations made twice each day (early afternoon and on retiring) 
should ordinarily be sufficient. In heavily tick-infested areas, 
however, or in sections known to be particularly dangerous, more frequent 
examinations should be made. When retiring, a complete removal of 
clothing is desirable. Both clothing and body should be examined care- 
fully and, if possible, any clothing not worn at night should be so placed 
that any undiscovered ticks will be unlikely to crawl from the clothing 
to the bed. If two or more persons are together, they should assist 
one another in the examination. If the person is alone, the back and 
other portions of the body that cannot be seen should be explored with 
the hands, paying particular attention to the hairy portions. 
Ticks may be removed from man. and the domestic animals with the 
fingers, but a better plan is to ut>e a pair of small forceps or 
tweezers. With these the tick may be seized by the head, close to the 
skin, and easily removed. There is no danger of leaving the tick's head 
imbedded in the skin. Care should be exercised against crushing the tick, 
as the contents of infected ticks are dangerous. After removing or 
handling ticks, the hands should be washed thoroughly with soap and water. 
Two or three inoculations of the tick emulsion vaccine give a 
degree of protection usually sufficient to last through one tick season, 
but the immunity apparently is not permanent. Occasional cases of 
spotted fever have developed in vaccinated persons, but the vaccine 
apparently lessens the severity of the disease and seems to insure 
recovery. For its full protective value the vaccine should be taken at 
least 10 days before exposure to tick bite. THE RICKETTSIAL DISEASES 
Introduction 
The Rickettsia diseases are acute infections characterized by high fever, 
a maculo-papular eruption which hecomes petechial, headache, and stupor. They 
are all transmitted in nature hy arthropods (lice, ticks, fleas, or mites) 
either directly from man to man or from rodent reservoirs to man. These dis- 
eases may he divided in two general groups, typhus fever and Rocky Mounts in 
Spotted Fever. They appear to he variants of the same disease. 
Causative Organisms 
The Rickettsiae are very minute, pleomorphic, cocco-haclllary organisms, 
smaller than the ordinary bacteria. They stain well only with the Romanowsky 
stains (Giemsa, Wright, etc.). They have never been cultivated on artificial 
media, but have been cultivated in tissue cultures, and on chick embryos. 
They are too large to pass through a Berkfeld filter. In man they multiply 
mainly or only in endothelial or mesothellal cells, in the arthropod mainly 
or only in the epithelial cells of the intestine. 
The Rickettsiae were discovered in 1910 by Ricketts and Wilder in the 
intestines of lice which had fed on typhus patients in Mexico. Later Ricketts 
found similar bodies in the blood of patients with Rocky Mountain Spotted 
Fever, and Wolbach found them in endothelial lesions of experimental animals. 
The question frequently arises as to whether the Rickettsiae are bacteria 
or ’virus particles". The question cannot be answered at present but the 
following seems to be a fairly tenable view. 
"The Rickettsiae are living organisms whose obligate intracellular para- 
sitism indicates a primary inability to metabolize foodstuffs" 
TYPHUS FEVER 
Causative Organism. - Eickettsia prowazekl. 
Synonyms. - Camp Fever, Jail Fever, Ship Fever, Spotted Fever, Famine 
Fever, Typhus Exanthematicus, Tabardillo (Mexico), Brill's Disease (New York) 
Varieties. 
1. Epidemic Typhus, more severe, higher mortality, transmitted by 
the louse (Pediculus humanus); occurs in epidemics usually starting in winter; 
associated with poverty, filth, war and famine; rare in the tropics. 
2. Endemic Typhus, less severe, very low mortality, transmission by 
rat flea, affects higher class of people or people working with grain or 
cattle or in clearing underbrush; not epidemic, but occurs most often in 
warmer months, common in the tropics. Endemic typhus is probably a variant 
of epidemic typhus modified by passage through the rat. This is the type 
of typhus fever in Texas. EPIDEMIC TYPHUS 
Historical 
The disease probably existed in ancient times but was first carefully 
described during the sixteenth century by two Italian physicians. From that 
time on it is known that typhus caused frequent devastating epidemics in' 
Europe and was one of the chief causes of death until the middle of the nine- 
teenth century* It was first clearly differentiated from typhoid fever in 
l837« In the United States it has never reached serious epidemic proportions, 
though introduced often by immigrants. During and after the World War there 
were terrible epidemics in the Balkan States, Poland and Russia, but there 
were very few cases in the armies of Britain, Germany, France or the United 
States. In 1909 it was proved that the disease is transmitted by the body 
louse. 
Geographical, Seasonal Incidence and Transmission 
These three factors are related because of the biology of the transmit- 
ting agent, the body louse (Pedlculus humanus, var. corporis). It lives close 
to the skin in the clothes,.and favors a temperature of about 90°F. It stays 
closer to the skin in cold weather, but crawls outside in warm weather, or if 
its host has a high fever as in typhus. It is less abundant in summer when 
thin or no clothing is worn. Having become Infected from a typhus patient in 
the period of onset, it leaves him in the high fever period and seeks a cooler, 
normal host. The louse feeds only on man. Epidemics, therefore, occur usually 
in temperate or cold climates, start in winter, and die out in summer. The 
epidemic disease is now found only in backward countries where pediculosus 
vestimente is common. The louse, once infected, remains so throughout its life, 
which lasts up to lays- The virus has been recognized in the louse only in 
the intestine. It has not been determined whether infection is acquired direc- 
ly from the bite of the louse, or only from scratching after a bite, louse 
excreta having been deposited on the skin. ' 14any medical attendants become in- 
fected during epidemics, often without knowledge of having been bitten by a 
louse. Either the louse is very elusive, or Infection may be acquired from 
louse excreta transferred from the body or clothes of a patient. 
Mortality 
Varies greatly ( 2-50per cent) in different epidemics and different popu- 
lation groups. Higher social classes when Infected usually have a higher mortality 
Prevention 
Depends entirely upon anti-louse measures. 
1. Delouslng 
The louse and its eggs are easily killed by a dry heat of 55°C. for 
five minutes, or by a moist heat of 70°C. for 50 minutes. Of chemicals, 
kerosene is much the most efficient. Cyanide, naphthalene, carbon disulphide 
and ammonia are also used. The louse is the most resistant of insects to 
fumigation. Ten ounces of sodium cyanide per 1000 cubic feet of air space with 
two hours exposure is required. Sulphur dioxide and formaldehyde gases are of 
no value. For clothing, heat is usually used. The ''Serbian Barrel" was im- 
provised to provide live steam. Closed shacks with a wood fire burning Inside 
are also used. Pressing seams of clothes with a hot iron may be employed, as 
eggs are usually laid on loose ends of cotton or wollen threads. Eggs are sometimes attached to tody hairs (the head louse P. humanus var capitis, may 
also transmit the disease). A typhus patient or healthy host of the louse is 
test deloused hy 
(l) shaving all hair 
(2) a hath of soap and kerosene 
(5) an entire change of clothing 
(U) female patients with head lice should have 
the hair washed first with Tincture of 
Delphinium and later with hot vinegar to 
loosen the eggs, which should then he comhed 
out with a fine-toothed comh. 
After thorough delousing and bathing, a patient is not a source of danger 
to others, and can he treated in a general ward. 
2. Protection Against Lice 
Attendants handling typhus patients or suspects must wear a louse- 
proof garment. This should he open only at neck and wrists and should he pro- 
vided with feet and soles so as to cover the shoes. Wrists should he tied with 
tapes or better fastened hy adhesive plaster. Cotton or rubber gloves tucked 
into sleeves of gown should he worn. Garment should he tied snugly about neck, 
such precautions, though extreme, have been found necessary during epidemics. 
ENDEMIC TYPHUS 
The Mexican Indians are said to have had a typhus-like fever before the 
discovery of America. After the conquest hy Cortez the disease was called 
'Tahardillo," the old Spanish name for typhus. It has continued in Mexico 
until the present time and exists in Peru, Bolivia, Chile and Argentina. 
Ricketts studied it and first described "Rickettsia" in Mexican cases. In 1925 
cases similar to it were found in the Rio Grande Valley and since then in prac- 
tically all of the Southeastern States; the Incidence has slowly Increased. 
They have occurred in people not infested with lice, in the upper and middle 
classes, and especially in people handling grain. A number of cases have occurred 
in professional men. The disease occurs in the tropics at all seasons, in the 
temperate zones only in the warmer months of the year. Direct transmission from 
man to man does not occur. As the result of epidemiological studies, it was 
concluded that there was probably a rodent reservoir of the disease, presumably 
rats or mice, and that man became "accidentally" infected from the bite of some 
ectoparasite of the rodent, either flea, mite or possibly tick. In February 1931, 
Dyer and Badger of the United States Public Health Service reported the produc- 
tion of typhus fever in guinea-pigs Injected with ground-up fleas from wild rats. 
In July 1931, Mooser, Castenada and Zinsser reported the production of typhus 
fever in guinea-pigs by the Injection of an emulsion of brain tissue from black 
rats caught in a prison in Mexico City. In October 1951 Dyer and other reported 
the experimental transmission of typhus in laboratory rats by the bite of the 
rat flea, Xenopsylla cheopis. Meanwhile Shelmire and Dove, in June 1951, reported 
the transmission of the disease in guinea-pigs by the bite of the tropical rat 
mite, Liponysus bacoti. They also showed that the causative organism could be 
transmitted to the next generation of mites through the egg. They believe that 
the epidemiology of the disease favors mite transmission rather than flea trans- 
mission. Their work, however, has not been confirmed. In October 1951, Mooser, 
Castenada, and Zinsser reported the transmission of typhus from rat to rat by the rat louse. This insect may he important in rat-to-rat transmission, hut it 
does not hite man. Thus the rat seems to he incriminated again as a reservoir 
of human disease, and the eradication of the disease can hast he achieved by 
the eradication of the rat. 
Prevention. - Avoidance of contact with rats, rat-proofing of buildings 
and the extermination of rats are the obvious methods of prevention. A vaccine 
has been prepared hut it is still in the experimental stage. 
Typhus is rapidly becoming a very important public health problem in Texas 
During the year Just passed, 1939, there were 558 cases reported to the State 
Health Department, the highest incidence in the history of the disease in this 
state. The mortality rate is now approximately that of typhoid. YEARS OF AGE 
DEATHS FROM CANCER IN TEXAS 
IN 1938 
BY AGE 
TOTAL DEATHS- 4650 
KEY- EACH MAJOR GRID 
REPRESENTS 40 DEATHS CANCER MORTALITY 
IN TEXAS 
1937 
TOTAL CANCER DEATHS 1937 
4,370 CANCER 
How shall we protect ourselves against cancer, the greatest of all the 
natural hazards in the adventure of living? Generally, like old age, cancer* 
is the result of the wear and tear of the tissues, due to the natural stresses 
of living. Unlike senility, cancer attacks the young much more frequently 
than is commonly realized and it plays the greater havoc the younger the sub- 
ject. If an ounce of prevention is generally worth a pound of cure, who may 
measure the value of cancer prevention? Yet prevention does not form a pro- 
minent chapter in the literature of cancer. It has not “been dignified, 
like cancer therapy, hy decades of acrimonious debate in medical societies. 
Nevertheless there is a great deal more to be done in the prevention of cancer, 
and most of it must be done by the person himself. 
For many years the cancer death rate has been rising until now it stands 
second only to heart disease and accidents as a cause of death in Texas. 
We are all more or less familiar with the cancer problem from the scien- 
tific standpoint. That is, it is produced in areas or organs subjected to 
chronic irritation, that it is more predominant in later adult life, it is 
extremely fatal, and the treatment is usually surgical combined with some ray 
therapy. 
Also, we have much of the cancer problem from a national angle. We wish 
to discuss the problem with you Texans as it relates to Texas. We want to 
review the records with you and tell you the story of the influence of cancer 
on the death rate of Texans as revealed by the death certificates filed in 
the State Department of Health. 
Let us go back sixteen years to 1925- That year we had an estimated 
population of 5,095,516 and there were 1605 deaths reported as from cancer. 
To avoid a long list of figures we may say that there has been a steady in- 
crease in cancer deaths until 1958, the last year for which complete figures 
are available, when there were L55O reported. However, this does not give 
the true picture. There were more people in Texas in 1958 than in 1925 to 
be subjected to the cancer menace, so it is necessary to use another yard- 
stick. In 1925 sixteen hundred and five out of a total of 5,059,652 people 
died of cancer, or for every 100,000 of our population 51*7 persons died. 
This we speak of as the cancer death rate for that year. Now, in 1958 our 
estimated population was 6,259,000 and died establishing a cancer 
death rate for that year of 72.6. 
There are several reasons as to why cancer has an increasingly high 
death rate, one, of course, being the lack of information on the part of the 
public as to the nature and course of cancer, and another is the fear of the 
disease and the tendency to put off medical care for fear that the physician 
will find that the disease or trouble is in reality a cancer, and still 
another is the fact that public health efforts toward the control of com- 
municable deaths in childhood has prevented a great number of deaths at this 
age. Thus, furnishing a greater population in those age groups in which cancer 
often appears. 
Going back over these 15 years month by month, we see no evidence of 
any seasonal variation and reports by counties snow no sectional predominance. 
The deaths appear distributed in proportion to the population except in cen- 
ters where hospitals drew from wide areas, and efforts at distributing these 
deaths back to the community of origin further bears out the conclusion that no areas are more affected than others. Although all elements of our popu- 
lation are affected by cancer it appears that the white race is slightly more 
susceptible than are the other races. They who comprise 75*5 Per cent of the 
population accounted for 85-5 per cent of cancer deaths and all other races 
16.5 per cent. The negro race which comprises 14.7 per cent of the population 
has 11.5 per cent of cancer, and the Mexicans which comprise 11.7 per cent only 
account for 5 per cent of cancer. 
Let us look at the problem from the standpoint of the organs of the body 
most usually affected. We find that cancer attacks any tissue or organ of the 
body, but fatal cases occur in order of their frequency in the following manner 
1. Intestinal tract 
2. Stomach 
5. Uterus 
k. Liver 
5. Male G-U organs 
6. Breast 
7. Skin 
8. Mouth cavity 
9. Respiratory system 
10. Female Genital organs 
We find that cancer deaths appear in the first year of life and gradually 
increase in number up to age 25 where it plays a dominant part in the total 
causes of deaths through the remainder of life's span, reaching its peak dur- 
ing the age period of 65 to 69 and rapidly declining to the age period of 95 
to 99* This study brings out one fact which is little considered and that is 
that after the first year of life cancer remains one of the fifteen leading 
causes of death throughout our existence. Conclusively illustrating the fact 
that no age is free from the menace and that any program to be wholly success- 
ful must include the total population instead of just those age groups where 
cancer deaths appear in great numbers. 
Cancer as a disease is a public health problem and responsibility because 
it affects relatively large numbers of people, because its frequency as a cause 
of death is on the increase and because systematized social action seems neces- 
sary in solution of the problem. An analysis of the foregoing statement cer- 
tainly reveals that any State Department of Health should be vitally concerned 
in the promotion of a cancer control program, since the work of such an organi- 
zation is concerned with the prevention and control of disease and the promo- 
tion of positive good health among citizens of the state. There is some 
doubt as to Just how far the State Department of Health of Texas should go into 
the promotion of such a program. We are, however, convinced that the following 
three essentials of cancer control should be carried on in every community in 
Texas and should be to a certain degree supervised through the State Depart- 
ment of Health: 
1. A dissemination of information to all the public concerning the 
early symptoms of the disease. 
2. Provisions for early diagnosis by competent specialists 
5. Adequate facilities for treatment 
The function of the State Health Department is to disseminate freely 
throughout its jurisdiction a thorough knowledge as to early warning signs 
of cancer. Educational material, if properly submitted, may be supplied with- 
out the danger of developing a cancer phobia. Such knowledge should be common 
among all people Just as the knowledge concerning the value of anti-toxin for 
diphtheria. 
It is an evident fact that something needs to be done in Texas if we expect to make any progress in reducing the death rate from this dreaded dis- 
ease. Since the Texas State Department of Health is now operating on a very 
limited appropriation, it is not difficult to understand why we have teen con- 
fined to only a limited educational phase of a cancer control program. 
In carrying forward this educational program, the State Department of 
Health has utilized newspapers, radio stations and free literature through 
which certain salient points concerning the disease are impressed upon the 
general public. The ordinary danger signals such as lumps in the breast, un- 
explained indigestion, loss of weight, chronic ulcers, pigmented moles, etc., 
are called to the attention of those who were interested and due emphasis has 
been placed upon the wisdom of periodic and thorough medical examination of 
individuals in whom these danger signals have appeared. The Department has 
also repeatedly called to the attention of the general public that hope for 
recovery from cancer depends upon early diagnosis and appropriate treatment. 
Among the difficulties confronting our educational program are lack of 
interest on the part of the public and human dread of learning that cancer is 
present. In many instances, none of the danger signals show themselves until 
the condition is far advanced. Many physicians are inadequately equipped hy 
knowledge, experience, and facilities to make a complete examination and 
diagnosis, or, in certain types of cancer, do not have necessary equipment 
for adequate treatment of the case. Finally, it must he admitted that even 
in the best circumstances there are definite limitations as to what can be 
done for the patient. 
The degree to which the State Department of Health will participate in 
the future program of cancer eradication will depend largely upon finances, 
public interest, and public demand. We desire to impress upon you that we 
stand ready to assist the American Society for the Control of Cancer and every 
practicing physician in any possible way in their united effort to control 
this great killer of our people. At all times the work of the Department is 
planned to be in close harmony and accord with the organized members of the 
medical profession. The question of Cancer Control must be approached in 
much the same manner as we have approached those of typhoid fever, diphtheria, 
malaria and as we are now approaching the question of syphilis control. We 
have now institute a program whereby cancer diagnostic service is available 
to physicians of T'exas through biopsy studies at the State Laboratory.