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Chapter 12

Table of Contents

Chapter 12

Malaria: Epidemiology

Colonel O Neill Barrett, Jr., MC, USA (Ret.)


Of the four species of malarial parasites affecting humans, three have been found in Vietnam: Plasmodium falciparum, Plasmodium vivax, and Plasmodium malariae. While P. falciparum and P. vivax are endemic throughout the country, P. falciparum is hyperendemic in the Central Highlands. P. vivax and P. malariae occur in greater proportions along the coast and in the delta (Nowosiwsky 1966). 

At least 11 species of anopheles mosquitoes have been identified as vectors in the transmission of human malaria (table 39). Anopheles minimus, A. jeyporiensis, and A. balabacensis are important in the mountains and forests while A. sundaicus and, to a lesser degree, A. minimus are important along the coast and in the Mekong Delta. A. maculatus is found only in the high plateau areas (map 6) (Kiel 1968; Stojanovich and Scott 1966).

When the rainy season begins in the highlands, the density of A. minimus increases. The breeding environment becomes unfavorable for this species as the rain increases in amount and force and the vector's density then decreases. A. jeyporiensis, which breeds effectively during the period of heavier rainfall, appears next. As the rainy season ends, this vector's density drops, in conjunction with increasing levels of A. balabacensis. The latter species seems to be the most important vector for the mountain-plateau regions, according to epidemiological observations (Nowosiwsky 1966, p. 32).


During the early buildup of the American forces in Vietnam, between March 1962 and February 1963, 20 cases of malaria were treated at the 8th Field Hospital in Nha Trang. Nineteen of these were caused by P. falciparum and 1 by P. vivax.* During 1963 and 1964, 59 patients were hospitalized and treated. In 1965, as the buildup increased and units became engaged in inland tactical operations, 1,972 cases were recorded (Kiel 1968, pp. 6-7). The largest number of cases was seen during 1967 and 1968 (table 40), although the rate-expressed as


* Maj. O'Neill Barrett, Jr., USARV Medical Consultant, Mar. 1962-Feb. 1963: Unpublished data.


TABLE 39.- Distribution and relative importance1 of Anopheles species as malaria vectors in Vietnam

number of admissions per 1,000 average strength per annum -showed a progressive decline from 98.4 per 1,000 per year in December 1965 to an average of 30 per year in 1969 (chart 13). From 1965 to 1970, a total of 78 deaths from malaria were recorded, an average of 13 per year (Neel 1973, p. 39).

Malaria rates have been shown to correlate with region of operation, climatic conditions, degree of contact with the enemy, proper use of malaria prophylaxis, and effectiveness of malaria discipline at the command level (Neel 1973, pp.37-40). That region of operation is important is verified by the observation that, in Vietnam, very little transmission of malaria occurred in Army base camps or around cities and large towns, most of which had active insect control programs (Nowosiwsky 1966, p.33), while large numbers of cases were reported from mountain and forest areas and from the Central Highlands (USARV-CHR 1967). The geographic distribution for the 8-month period of July 1967 to February 1968 is shown in map 7. This distribution generally is applicable to 1966 as well (map 8). Using such general epidemiological data along with local and regional malaria surveys, unit medical officers were able to compile experience maps of their sectors which helped them to estimate the number of malaria cases to be expected. A typical example is the map compiled by the division surgeon, 1st Cavalry Division, for the period of September 1965 to December 1966 (fig.70).

Degree of contact with the enemy also had a marked effect on the incidence of new cases of malaria. In March and April 1966, the 1st Cavalry Division conducted field operations in hyperendemic areas, including Operations JIM BOWIE (13-21 March, in the Bong Son valley), LINCOLN (25 March-8 April, in the Ia Drang valley), and MOSBY (beginning 11 April in the southwest Kontum Province). The 1st and 3d Brigades of the division were involved in these operations while the 2d Brigade patroled highway 19 and held the perimeter at An Khe. Following the first two operations, the 1st Brigade sustained 204 new cases


Map 6. – Distribution of proven and suspected malaria vectors in Vietnam. (Kiel, F. W. 1968. Malaria in Vietnam. In Pathology Annual, ed. S. C. Sommers, pp. 1-27. New York: Appleton-Century-Crofts.)


TABLE 40.- Total cases and deaths caused by malaria, U.S. Army, 1966-70

CHART 13.- Admissions to hospital and quarters for malaria among U.S. Army personnel in Vietnam, 1965-69

of malaria and the 3d Brigade had 104. Onset of the increase in incidence was shown in each instance to occur 14 days after the midpoint of an operation, corresponding to the usual 10- to 14-day incubation period for falciparum malaria. The 2d Brigade recorded only 12 new cases during the same period (USARVMC).

Another example is the experience of a Special Forces Mobile Strike Force company, during Operation PAUL REVERE IV, November-December 1966. Chart 14 shows that five cases occurred early in the operation, whose date of onset precluded acquisition in the operational area. Subsequently, however, 43 cases were diagnosed. The first of these cases occurred 12 days after first exposure to the area and the last case 15 days after last exposure. The majority of


MAP 7.- Geographical occurrence of malaria, 29 February 1968. (USARV surgeon. 1968. Monthly Command Health Report to USARV commander, Feb. 1968)


MAP 8.- Relative malaria endemicity in Vietnam, 1966 (Kiel, F.W. 1968. Malaria in Vietnam. in Pathology Annual, ed. S.C. Sommers, pp.1-27. New York: Appleton-Century-Crofts.)


FIGURE 70.-Malaria experience, 1st Cavalry Division, September 1965-December 1966. (Kiel, F.W. 1968. Malaria in Vietnam. In Pathology Annual, ed. S. C. Sommers, pp. 1-27. New York: Appleton-Century-Crofts.)

cases occurred between 10 and 14 days after midpoint of exposure (Cottingham, Boone, and Legters).    

The role of enemy contact is further emphasized by the distribution of cases by MOS (military occupational specialty). Of all cases of malaria reported in 1967 in the U.S. Army, Vietnam, 58.5 percent occurred in individuals with the 11B (light weapons infantryman) MOS, although persons with this specialty represented only 15.3 percent of the total strength (USARV-CHR 1967, table 2).

Malaria discipline and the proper use of malaria chemoprophylaxis are discussed in chapter 14.


Scant data are available concerning malaria in enemy troops. A U.S. Army Medical Intelligence report compiled during 1965 suggested that it was a significant cause of noneffectiveness in some units (Killenberg 1965). One NVA (North Vietnamese Army) officer told interrogators that between February and June 1965 his company of 113 men had lost 34; 11 were killed in action and 23 died from malaria. This unit had traveled along the Laotian border into the Central Highlands and engaged in operations in Darlac, Phu Bon, Pleiku, and Binh Dinh Provinces. In November 1965, 12 captured NVA soldiers were examined and 8 were found to have blood smears positive for P. falciparum. They had been in combat near Pleiku and had been in the Republic of Vietnam for 2½ months. On


CHART 14.-Morbidity from malaria by date of onset, related to activities of one indigenous company in connection with Operation PAUL REVERE IV, Vietnam, November-December 1966

the other hand, only 3 of 113 VC (Vietcong) prisoners captured in Binh Tuy Province had positive smears. These captives were local VC popular force personnel, most of whom were not normally engaged in field operations.

Information about the prophylaxis used by enemy forces is even less complete. A container removed from the body of an NVA soldier near Pleiku in November 1965 contained 20 tablets of quinacrine. A captured main force soldier described taking "two pills of quinine a day for 24 days a month." Another captured infantry private indicated that each soldier received 100 antimalarial pills as part of his basic issue. These data suggest that VC field elements did attempt to suppress malaria with oral medication. Lack of uniformity may have been the result of differences in the availability of drugs as well as variations in medical policy (Killenberg 1965).


Anopheline infestation without malaria probably existed before the exploration and settling of North America. It is likely that the disease was brought to the East Coast by early settlers from certain swampy counties in England and to the Gulf Coast by French and Spanish settlers. An increase in incidence occurred with the importation of slaves from Africa. Malaria was at a peak in the United States by 1855, when it had become endemic throughout the country and hyperendemic in the southeastern states (Duffy 1953, pp. 204-14; Lisansky 1958). 

During the next century, the incidence of malaria gradually declined as a consequence of social and economic changes and organized malaria eradication programs. By 1956, endemic malaria had virtually disappeared in the United States (Lisansky 1958, pp. 437-38). The decline of the disease was temporarily reversed when infected troops returned from overseas, most notably during and immediately following World War II and the Korean war (Fisher et al. 1970).

United States involvement in Vietnam led to a predictable rise in imported cases of malaria in this country (NCDC-MS68; Barrett 1968), because of the increased number of troops assigned there, failure of prescribed prophylaxis pro-


grams, and drug resistance in some cases (Barrett and Reiley 1971). In 1965, 156 cases were reported in the United States and Puerto Rico (NCDC-MS65); in 1970 the number had risen to 3,997 (Walter, Dover, and Schultz 1972). The progressive increase during this period is shown in chart 15. Military personnel, including recently discharged veterans, accounted for almost all of the upsurge; incidence in civilians remained constant. Most of the military cases occurred in Army personnel (table 41).

Although both troops in Vietnam and returnees to the United States experienced an increase in cases, a striking difference between the two groups was noted. Of those cases which developed in Vietnam during the early years of the war, 98 percent were caused by P. falciparum infection (Sheehy 1967). However,

CHART 15.- Cases of malaria in the military and civilian populations, United States, 1959-70


TABLE 41.- Malaria in military personnel returning from Vietnam to the United States, 1970

P. vivax infection was responsible for 83 to 93 percent of the cases which occurred in the United States (Waterhouse and Riggenbach 1967; Martelo, Smoller, and Saladin 1969).

In Vietnam, all individuals were supposed to receive weekly C-P (chloroquine-primaquine) prophylaxis, which is highly effective in suppressing vivax malaria (JAMA) but less effective against P. falciparum (Blount 1969). Each individual was also instructed to take one C-P tablet weekly for 8 weeks following return to the United States. This program should have resulted in radical cure of P. vivax infection, thus virtually eliminating vivax cases in the United States (Barrett and Reiley 1971). The high incidence of vivax malaria observed suggested that either the drug program itself or the enforcement of it was ineffective. There was no evidence to support the first possibility (USMED). On the other hand, Barrett (1968) found that, of 29 patients with vivax malaria treated at Letterman Army Hospital in San Francisco, none had completed the prescribed 8-week treatment regimen or maintained treatment until onset of symptoms.

This observation led to a study of 671 asymptomatic Vietnam veterans to determine the degree of participation in the prophylactic program (Barrett et al. 1969). Overall results are shown in table 42. The most striking finding was that 70 percent of all individuals had failed to complete the prescribed course of malaria prophylaxis upon return to the United States. A variety of reasons were given (table 43). Although 20 percent noted side effects from the therapy, only 11 percent gave this as the reason for discontinuing it. Rank was not a factor, as the failure rate was similar for officers and enlisted personnel. Persons stationed in "high risk" areas were more likely to comply with therapy than were those in locations where the disease was not a significant epidemiological problem. On the other hand, previous experience with malaria provided little stimulus to comply, as 76 percent of those who had clinical disease in Vietnam failed to complete treatment when they returned to this country.

The practical impact of imported malaria on a military unit in the United States was demonstrated by Di Napoli and Dicey (1969). During the winter and spring of 1966-67, there was a sharp increase in the incidence of malaria at Fort Bragg, N.C., and during 1967, 353 cases occurred, 274 (77.6 percent) of them in personnel of the 82d Airborne Division. With an average stay of 14 days per pa-


TABLE 42.- Results from malaria chemoprophylaxis survey of 671 U.S. servicemen returned from Vietnam

TABLE 43.-Reasons given by 470 U.S. servicemen returned from Vietnam for failure to complete therapy in malaria chemoprophylaxis survey

tient at Womack Army Hospital, these cases represented a total of 3,836 mandays lost and an estimated monetary cost of $204,600 to the division. Extrapolating these data to the overall incidence of malaria in the U.S. Army in 1967, the authors estimated fiscal loss from the disease to be $1.8 million.

The return of large numbers of troops from malarious areas also raised the question of introduced malaria (malaria acquired by mosquito transmission from an imported case in an area where the disease is not a regular occurrence). For successful mosquito transmission of malaria, three ingredients are necessary: a susceptible population, a parasite reservoir, and an effective anopheline vector; all three exist in the United States. The reservoir is provided by infected individuals who return from malarious areas. Anopheles freeborni is an efficient


vector in the western half of the country and Anopheles quadrimaculatus in the eastern half. Introduced malaria has, however, been uncommon in the United States, apparently because of improvements in standards of land use and housing, together with increased urbanization and a concomitant decline in the rural population, all factors which tend to separate man from mosquitoes and, in many instances, promote an adverse environment for the anopheline vector (Barrett 1968, p.431).

Nonetheless, introduced malaria has been documented in this country. In 1952, 35 cases occurred among a group of Camp Fire Girls in California. The probable source was a recently returned Korean veteran (Brunetti, Fritz, and Hollister 1954). At Fort Benning, Ga., two cases of introduced vivax malaria were observed in 1964 and 1965, the probable source again being a serviceman who had been stationed in Korea (Luby et al. 1967). There is evidence of at least one instance of introduced vivax malaria resulting from exposure to a person returned from Vietnam (ABNEWS). In 1970, two introduced cases were reported from rural., south-central Texas where a migrant Mexican agricultural worker was the probable index case (Walzer, Dover, and Schultz 1972, p.195). Between 1952 and 1974, a total of 11 outbreaks of introduced malaria in the United States were reported to the Center for Disease Control. P. vivax was the species identified in all of the cases (CDC 1974).

Of perhaps greater significance than introduced malaria in the United States is induced malaria (malaria acquired through artificial means, especially via blood transfusion or the use of common syringes and needles).

Gubb (1919) reported what was probably the first case of transfusion-induced falciparum malaria 8 years after the danger of transmission of malaria by transfusion was first recognized (Belding 1965, p. 313). The first case of transfusion-induced falciparum malaria from a Vietnam returnee in the United States was reported by Chojnacki, Brazinsky, and Barrett (1968). This case was of interest for two reasons. First, investigation established that the source of infection was a soldier who had returned from Vietnam 7 months previously and had never had symptoms of malaria. Equally significant was the fact that routine evaluation of this individual, during the attempt to establish the source of the infection, was unrewarding. Twenty-four thick and thin smears done at least 1 day apart were negative for malaria. Diagnosis was based on parasite identification in a sternal bone marrow aspirate. Belding (1965, p. 307) had previously commented on the value of marrow aspirate evaluation in confirming clinically suspected cases with negative peripheral smears.

Forty cases of transfusion-induced malaria were reported in the United States from 1963 to 1974. P. vivax was the cause of 16 (40 percent) of these, P. falciparum, of 13 (32 percent), P. malariae of 10 (25 percent), and a mixed infection of 1 (3 percent). Only one case of transfusion-induced disease was noted in the United States in 1975; this was a fatal case caused by P. malariae. Because only 1.4 percent of all malaria cases in the United States were caused by P. malariae while 25 percent of transfusion-related cases involve this strain, it is proportionately the most important cause of transfusion-induced malaria in this country (CDC 1976).


Theoretically, current routine blood banking restrictions prevent most cases of transfusion-induced disease by precluding donation of blood for 2 years after termination of treatment for, or known exposure to, malaria (AABB, pp. 9-10). However, some donors, particularly paid ones, do not provide honest information concerning previous exposure. Furthermore, there are well-documented cases with unusually long incubation periods, so that the 2-year restriction does not exclude all infected donors (NCDC-MS68). A practical indirect fluorescent antibody technique for detecting previous exposure to malaria is available. It is especially valuable for investigating febrile transfusion reactions but has not as yet been used routinely as a screening technique by blood banks (Leibovitz et al. 1969).

While whole blood is the greatest source of transmission of induced malaria, component therapy is also a potential hazard. There is one case report of transmission of P. vivax by leukocyte concentrate component therapy (Dover and Guinee 1971). The patient, who had leukemia, received leukocyte infusions from a Vietnam veteran. The component product was probably contaminated with parasitized erythrocytes.

Another documented cause of induced malaria is illicit parenteral drug use. Several isolated cases were reported from various parts of the country in 1970 and 1971 (Dover 1971). An epidemic of induced malaria involving 48 people occurred between December 1970 and March 1971, in Kern County, Calif. All patients were heroin users who frequently shared syringes and needles. The probable index case was a 22-year-old veteran who had returned from Vietnam in March 1970 and had taken none of the chemoprophylaxis tablets. He experienced a clinical attack of malaria in December. During the time between the onset of symptoms and diagnosis, he had injected heroin at least once daily and shared his injection equipment with at least seven persons, three of whom subsequently developed malaria. An epidemiological investigation was initiated and a special clinic was established by the Kern County Health Department to interview all contacts and suspected cases. Parasites of P. vivax were seen on the peripheral blood smears of 42 patients, and all had recent or current symptoms typical of vivax malaria (CDC 1971). The possibility of malaria should always be considered in the evaluation of fever in persons using illicit drugs parenterally.


AABB-American Association of Blood Banks. 1966. Technical methods and procedures of the American Association of Blood Banks. 4th ed. Chicago: Twentieth Century Press.

ABNEWS-Introduced malaria case identified. 1967. Antibiotic News 4: 1, 23 Aug. 67.

American Association of Blood Banks. See AABB. Antibiotic News. See ABNEWS.

Barrett, 0., Jr. 1968. The problem of vivax malaria in Vietnam returnees. Mil. Med. 133: 211-14.
Barrett, 0., Jr., and Reiley, C.G. 1971. Malaria-a problem for Hawaii? Hawaii M. J. 30: 27-30.
Barrett, 0., Jr.; Skrzypek, G.; Datel, W.; and Goldstein, J. D.1969. Malaria imported to the United States from Vietnam. Am. J. Trop. Med. 18: 495-99.

Belding, D. L. 1965. Textbook of parasitology. 3d ed. New York: Appleton-Century-Crofts.
Blount, R. E. 1969. Malaria-a persistent threat. Ann. Int. Med. 70: 127-29.

Brunetti, R.; Fritz, R. F.; and Hollister, A. C., Jr. 1954. An outbreak of malaria in California, 1952-1953. Am. J. Trop. Med 3:779-88.

CDC -Center for Disease Control, Department of Health, Education, and Welfare. Morbidity and Mortality Weekly Report 20: 99-110, 27 Mar. 1971; 23: 285-87, 17 Aug. 1974; 25: 125, 30 Apr. 1976.

Chojnacki, R. E.; Brazinsky, J. H.; and Barrett, 0., Jr. 1968. Transfusion-introduced falciparum malaria. New England J. Med 279: 984-85.

Cottingham, A. J.; Boone, S. C.; and Legters, L. J. A prospective study of malaria incidence among indigenous and U.S. forces during combat operations. In Annual Progress Report, U.S. Army Medical Research Team (WRAIR) Vietnam and Institute Pasteur of Vietnam, 1 Sept. 1966-31 Aug. 1967, pp. 2-23.

Di Napoli, R. J., Jr., and Dicey, B. B. 1969. A study of malaria in the 82d Airborne Division, Fort Bragg, North Carolina, 18 July 1968. In Army Medical Service Activities Report, 1968, Headquarters, 82d Airborne Division. Report to commanding general, XVIII Airborne Corps, 27 Feb. 69.

Dover, A. S. 1971. Malaria in a heroin user. (Letter to the editor.) J.A.M.A. 215: 1987.

Dover, A. S., and Guinee, V. F. 1971. Malaria transmission by leukocyte component therapy. JA.M.A. 217: 1701-2.

Duffy, J. 1953. Epidemics in colonial America Baton Rouge: Louisiana State University Press.
Fisher, G. U.; Gordon, M. P.; Lobel, H. 0.; and Runcik, K. 1970. Malaria in soldiers returning from Vietnam. Epidemiologic, therapeutic, and clinical studies. Am. J. Trop. Med. 19: 27-39.
Gubb, A. S. 1919. Accidental transference of the malarial parasite in the course of transfusion. Brit M. J. 2: 74-75

Health of the Army. See HOA

HOA-Office of the Surgeon General, Department of the Army. Health of the Army, May 1965, May 1966, May 1967, May 1968, May 1969, and May 1970. Copies at Uniformed Services University of the Health Sciences.

JAMA-Malaria (Editorial). 1966. J.A.M.A. 195:308-9.
Journal of the American Medical Association. See JAMA.
Kiel, F. W. 1968. Malaria in Vietnam. In Pathology Annual, ed. S.C. Sommers, pp. 1-27. New York: Appleton-Century-Crofts.

Killenberg, Capt. Paul C., MC, 521st Medical Detachment (Intelligence). 1965. Preliminary Report on Malaria in Enemy Troops, 28 Dec. 65.

Leibovitz, A.; Freeborn, F. R.; Lillie, H. J.; Houston, W. E.; Smith, C. D.; and Goldstein, J. D. 1969. The prevalence of malarial fluorescent antibodies in Vietnam returnees with no history of overt malaria. Mil. Med 134:1344-47.

Lisansky, E. 1958. The eradication of malaria as an endemic disease in the United States. Ann. Int. Med. 48: 428-38.

Luby, J. P.; Schultz, M. G.; Nowosiwsky, T.; and Kaiser, R. L. 1967. Introduced malaria at Fort Benning, Georgia, 1964-1965. Am. J. Trop. Med 16:146-53.

Malaria surveillance, National Communicable Disease Center. See NCDC-MS.

Martelo, 0. J.; Smoller, M.; and Saladin, T. A. 1969. Malaria in American soldiers. Arch. Int. Med 123:383-87.

Morbidity and Mortality, Center for Disease Control. See CDC.

NCDC-MS-National Communicable Disease Center, Department of Health, Education, and Welfare. Malaria surveillance. Annual Summaries, 1965, 1968.

Neel, S. 1973. Medical support of the U.S. Army in Vietnam, 1965-1970. Vietnam Studies. Washington: Government Printing Office.

Nowosiwsky, T. 1966. Some epidemiologic considerations of malaria in U.S. personnel in Vietnam. USARV M. Newsletter, Mar., pp. 30-34. Copy in Joint Medical Library, Office of the Surgeons General.

Sheehy, T. W. 1967. Malaria in servicemen from Vietnam. Ann. Int. Med 66: 447.

Stojanovich, C. J., and Scott, H. G. 1966. Illustrated key to mosquitoes of Vietnam. Atlanta: National Communicable Disease Center, Department of Health, Education, and Welfare.

USARV-CHR-USARV surgeon. Monthly Command Health Report to USARV commander. Dec. 1967, Feb. 1968. On file at U.S. Army Center of Military History.

USARV-MC-USARV medical consultant. 1966. Monthly report to USARV surgeon, Apr. 66.
USARV medical consultant. See USARV-MC.

USARV monthly Command Health Reports. See USARV-CHR.

USMED-Malaria cures highest with combined drugs. 1967. U.S Med 3:14-16, 1 June 67. U.S. Medicine. See USMED.

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