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Chapter 8

Contents

CHAPTER VIII

Trachoma

Thomas G. Ward, M.D., Dr. P.H.

Trachoma is a contagious disease of the eye which is caused by an unidentified organism. The causative agent exemplifies some of the characteristics of both the viruses and the rickettsiae. The organism leads to local inflammation in the conjunctiva, both the tarsal and bulbar areas, and the local inflammation is characterized by the formation of granules, corneal ulcers, pannus, and, ultimately, scar formation with possible paralysis of the palpebral muscles.

EPIDEMIOLOGY

Soldiers returning from Africa during the Napoleonic wars introduced trachoma into Europe late in the 18th century.1 After the introduction, the disease rapidly spread to all of Europe and has maintained high endemicity in the Balkan States. It is now worldwide, and in some countries surveys have indicated that a large proportion of the population is affected. For example, in Egypt, 98 percent of the population is affected; in India, 75 percent; in Siam, 65 percent; and in both Malaya and Poland, 50 percent. The Indians in the United States had an incidence of about 26 percent in 1937, but by 1941, the judicious use of sulfanilamide had reduced this incidence to 3 percent.

There seems to be a racial type of immunity, or, rather, the agent may have an affinity for some races. Jews, Mongols, and Poles seem to have higher attack rates than do other Caucasians living in the same areas. Negroes seem to be affected only slightly, with the exception of those living in western Africa. Economic status may play an important role in the incidence of the disease, in that in Egypt the attack rates are highest among the lower economic levels. Two explanations offer themselves, neither of which has been proved experimentally: (1) Persons of low economic status have a poorer nutritional state, and, consequently, in these people the tissues of the eye are more susceptible and (2) the environment of lower economic groups is not so clean and the contact rate between patient and susceptible contact (usually infant) is correspondingly higher.

Formites play an important role in the transmission of the disease, in that mothers have been seen wiping the trachomatous material from their

1Murray, W. B.: A Review of Trachoma. Canad. M.A.J. 60 : 574-580, June 1949.


128

eyes and immediately cleaning the children's eyes with the same cloth. In addition, flies are probably important carriers, in that the swarms of flies noted in the eyes of Egyptian children are surely capable of physically transporting the infectious material to the eyes of susceptible playmates.

ETIOLOGY

The cause of trachoma (Chlamydozoa trachomatis) was discovered independently in 1907 by Halberstaedter and Prowazek2 working in East Prussia, and by Greeff, Frosch, and Clausen3 working in Java.

The Prowazek-Halberstaedter body is the inclusion found intracytoplasmically next to the nucleus. It measures approximately 3 by 13 microns and may contain smaller elementary bodies of the order of 250 millimicrons. The inclusion bodies stain blue with Giemsa's stain and the large-sized ones contain the elementary bodies which stain red with Giemsa's stain. The inclusion bodies are the pathognomonic sign but according to Stewart4 may be found in about 40 percent of the cases when one surveys all cases of trachoma. However, if examination is limited to early cases, then the inclusion bodies may be found in practically all cases.

Some workers consider the agent of trachoma as a rickettsia and list the following points as favoring such a view: Staining reaction with Giemsa's stain; cytoplasm of the host cell is filled with small, red staining bodies which are not restricted to a definite inclusion body; and no proof of insect parasitism for the Chlamydozoa for trachoma or related diseases has been forthcoming. Other workers5 believe the agent to be a virus, in that it is filterable and has not been grown on lifeless media.

The only laboratory animals which may be infected with certainty are the baboon and the grivet. This makes research in the disease all the more difficult, and most of the observations with respect to infectiousness have been made through the use of human volunteers. Stewart reported the agent as filtrable through collodion membranes of 0.6 to 0.7 micron average pore diameter. Titration experiments indicate that the infectious agent collects on the upper surface of the filter.

CLINICAL SYMPTOMS

The clinical findings in trachoma are confined to the eye. In the early stages there is photophobia, itching, and lachrymation, and patients complain of a scratching sensation in the upper lid. The disease progresses until the patient begins to notice an abnormality of the upper lid, in that

2Halberstaedter, L., and Prowazek, S. von : Über Zelleinschlüsse parasitärer natur beim trachom. Arb. a.d.k. Gsndhtsamte. 26 : 44-47, 1907.
3Greeff, Frosch, and Clausen : Untersuchungen über die Entstehung and die Entwicklung des Trachoms. Arch. f. Augenh. 58: 52-63, 1907.  
4Stewart, F. H.: The Aetiology of Trachoma. Brit. J. Ophthal. 23 : 373-380, June 1939.  
5Thygeson, P., and Proctor, F. I. : The Filtrability of the Trachoma Virus. Arch. Ophth. 13: 1018-1021, June 1935.  


129

it cannot be raised properly, or until he notices corneal ulcers and dimming of vision. It is at about this stage that the patient presents himself to a physician, but the damage that has been done is irreversible, and therapy can only stop the progress of the disease.

MacCallan6 has classified the disease into four stages, with clinical symptoms as follows:

First stage: Lymphocytic infiltration with or without lymphoid follicles. Usually located beneath the conjunctival epithelium.

Second stage: Conjunctival blebs or papillary hypertrophy as a complicating state.

Third stage: Scarring, with absorption of the lymphocytic infiltration.

Fourth stage: Complete cicatrization in the absence of apparent inflammation.

As the disease progresses from stage to stage, there is an early loss of normal gloss of the conjunctiva, followed by the slow subacute inflammation leading to a dark cherry color of the blood vessels lining the upper eyelid. The pannus begins at the upper pole of the limbus as a grayish white curtain which progresses downward into the pupil. The ulcer is located centrally in the cornea which is the point farthest from the blood supply. The final result is that the upper lid hangs downward over the pupil and the eyelashes are turned inward, scratching the eyeball, which is smaller in size than normal.

TREATMENT

The treatment of trachoma, as recommended by the Bureau of Indian Affairs, U.S. Department of Interior, is to administer sulfanilamide in doses of one-third grain per pound of body weight for 10 days and in doses of one-fourth grain per pound for the following 2 weeks. The incidence has been cut from about one-fourth to about one-thirtieth by a preventive sulfanilamide therapy as noted above. Local treatment with sulfonamides7 and penicillin8 has been reported as beneficial in this disease.

SUMMARY

Trachoma was not a serious disease in the Army during World War II. There was a total of 826 admissions for the disease reported during the years 1942-45 (table 13). These occurred as follows: 164 in 1942; 351 in 1943; 171 in 1944; and 140 in 1945. Approximately 538 admissions were reported from troops in the United States , the remainder from troops stationed overseas. Of the oversea areas, the Southwest Pacific Area and the Mediterranean theater (including North Africa ) reported the highest num-

6MacCallan, A. F.: Trachoma. London : Butterworth and Co., Ltd., 1936.
7Miterstein, B., and Stern, H. J.: Treatment of Acute Conjunctivitis and Trachoma With Sulfonamides. Lancet 1: 649-650, May 1945.
8Darius, D. J.: Penicillin Treatment of Trachoma. Am. J. Ophth. 28 : 1007-1009, September 1945.  


130

ber of admissions for trachoma. The highest admission rates were reported from the Middle East and Mediterranean areas. In all other areas, the number of cases was so small that no preventive medicine problem of any consequence was presented.

TABLE 13.-Admissions for trachoma in the U.S. Army, by theater or area and year, 1942-45

Theater of area

1942-45

1942

1943

1944

1945

Number

Rate

Number

Rate

Number

Rate

Number

Rate

Number

Rate

Continental United States

538

0.04

138

0.05

240

0.05

90

0.02

70

0.02

Overseas:

 

 

 

 

 

 

 

 

 

 

    

Europe

36

.01

1

.01

---

0

25

.01

10

.00

    

Mediterranean1

95

.06

3

.13

74

.16

14

.02

5

.01

    

Middle East

10

.07

---

0

6

.11

4

.09

---

0

    

China-Burma-India

11

.03

---

0

3

.08

8

.05

---

0

    

Southwest Pacific

73

.04

10

.14

5

.03

18

.03

40

.04

    

Central and South Pacific

38

.03

6

.04

9

.03

8

.02

15

.04

    

North America2

17

.03

5

.05

10

.03

2

.02

---

0

    

Latin America

5

.01

1

.01

2

.02

2

.02

---

0

         

Total overseas3

288

.03

26

.04

111

.07

81

.02

70

.02

         

Total Army

826

.03

164

.05

351

.05

171

.02

140

.02


1Includes North Africa.
2Includes Alaska and Iceland.  
3Includes admissions on transports.

Military personnel, or potential military personnel, who have had acute trachoma and who have been pronounced cured should be examined in an Army hospital to determine if cure has been effected; if it is established that a cure has been effected, the individual should be allowed to enter into, or to continue, military service without jeopardy.

Because the number of cases will, in all probability, be small, each person should be considered on an individual basis, and there appears to be no need to establish a policy governing the actions of medical officers in the Army

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