The Journal of Texas Medicine: July 2012

The Past and Present of Malaria in Houston 

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The Journal – July 2012

Tex Med. 2012;108(7):e1.

By Paola Carrasco, BS, and Wayne X Shandera, MD

From the Department of Internal Medicine, Baylor College of Medicine, Houston TX 77030. Ms Carrasco, fourth-year medical student; Dr Shandera, internist and faculty member. Send correspondence to Wayne X. Shandera, MD, Ben Taub General Hospital, 1504 Taub Loop, 4RM-81-001, Houston TX 77030; email:   


Malaria has a long-standing association among diseases that affect Texans and Houstonians. Early records show that in 1935 at least 25,000 cases of malaria were reported in Texas (with at least 1500 in Houston) and that between then and 1959 the largest number occurred in August. A dramatic fall in malaria incidence occurred through the 1930s and 1940s, with a surge at the onset of World War II and very few cases in the 1950s. Texas records report 625 travel-associated cases in Texas from 1952 through 1959. Another 115 case-patients were reported by combining data from Ben Taub General Hospital between 2003 and 2009 and from the City of Houston Health Department between 2005 and 2009. These cases manifested Plasmodium falciparum disease typically among travelers to Africa (85% of recent cases) or Plasmodium vivax among Central American immigrants. Only about one-half of these patients took prophylaxis, and only 1 patient (a Cameroonian) reported having used artemisinin combination therapy.  


Malaria was not present in the United States before colonization in the 16th and 17th centuries, at which time its area of involvement, akin to the settlers themselves, moved westward. The Spanish, English, Dutch, and French uniquely brought Plasmodium vivax and P malariae, while slaves from Africa, in particular, introduced P falciparum over the 200 years during which the slave industry prospered. According to Russell, "by 1776 malaria was widely prevalent" in many areas of the United States.1 The geographic area of malaria, however, did not retreat to the Southeastern United States until approximately 1850. The effects of malaria were profound as observed by Dr Carter, a prominent malariologist, who observed the loss of efficiency caused by the infection in the South and claimed that this loss surpassed that of any other disease at the time.2 The number of malaria cases showed a general decline until the disease was no longer endemic in 1951. The general trend downward during this time is typically attributed to a long series of efforts to eradicate it, particularly mosquito control and use of the agent dichlorodiphenyltrichloroethane (DDT).

Currently, 1500 cases of malaria are reported annually in the United States.3 Many of these are travel-related and, in particular, among locals who travel in return to homelands in Africa. In one year alone (2004), reports described 869,000 bidirectional visits between the United States and Africa.4,5 A study from New York6 confirms that a large portion of those infected acquire the organism in Africa and that few take appropriate prophylaxis.

The epidemiology of malaria in Houston, on the other hand, is not as well known. Because 30.4% of Houston residents are foreign born,7 because the city has an emerging large number of African national communities (including one of the largest Nigerian communities in the nation8), and because many of these residents travel often with their families to visit their home countries of record, a study of malaria epidemiology in Houston is needed.

A recent paper examined the epidemiology related to children with malaria, using cases reported between 1994 and 2007 in Houston.9 This report confirmed a scant use of appropriate malarial prophylaxis. These data did not examine adult cases. Malaria cases reported in Houston between 2003 and 2009 were assessed to determine the descriptive epidemiology of locally reported malaria in the hope of improving prevention and treatment.   


The Texas Department of Health provided weekly and yearly tallies of malaria cases for the interval 1935-1959 with travel-associated data available between 1952 and 1959. No specifics with respect to county or city of origin were available.

A retrospective chart review of malaria case-patients reported to Ben Taub Hospital between 2003 and 2009 and to the City of Houston Health Department between 2005 and 2009 was conducted. Case-patients included adults and children. Variables assessed included age, sex, countries where the disease was acquired, malaria speciation, prophylaxis administration and use, and type of treatment received. The data were analyzed by using Stata 11, particularly to test for trend, and Fisher's exact test.   


Case counts are available for Texas (but not for Houston specifically) between 1935 and 1959, documenting at least 25,000 per year in 1935 (with an estimated incidence of 417 per 100,000 person-years). The estimated case count from Houston in 1935 was at least 1500 as Houston had about 7% of the Texas population then (350,000/6,000,000 persons; and being in the more malaria-prone Southeastern part of the state, this number is an underestimate). The case loads showed that week 33 (mid to late August) was associated with the highest numbers of cases (Figure 1).

The incidence fell dramatically through the 1930s and 1940s, with an increase in the case-load in the early 1940s at the onset of World War II (Figure 2). Only sporadic cases were reported after about 1952.

The total number of travel-associated cases from 1952 to 1959 for the entire state of Texas was 625. Fifty-seven percent of cases were present in 1952 (386), followed by a later surge in 1954 (110).

Rare autochthonous cases were subsequently reported from Houston in the early 1990s,10 according to public health veterinarian James Steele, DVM, in a telephone interview January 13, 2011.

Houston cases include 115 case-patients reported from Ben Taub General Hospital (28 case-patients, 2003-2009) and the City of Houston Health Department (87 case-patients, 2005-2009).   Speciation was available for 93 (81%) case-patients and included 63 (67.7%) with P falciparum, 20 (21.5%) with P vivax, 9 (9.7%) with P malariae, and 1 with concomitant P falciparum and P malariae infection. Neither the number of P vivax or P falciparum cases changed significantly for the study interval 2005-2009 (P=0.33 [vivax] and P=0.27 [falciparum], test for trend).

The sex ratio among 83 case-patients with available data was 1.96 males to female (M:F). The mean age on presentation was 32.8 years (range, 1-78 years, SD 17.4) and the age did not differ significantly by gender. For P falciparum cases (n = 45), the sex ratio was 1.37 (M:F), and for P vivax cases (n = 16), the ratio was 4.33 (M:F) (P=0.08, Fisher's exact test). The age at onset of symptoms did not differ by species. Among 85 case-patients with data regarding origin of infection, 72 reported acquiring the infection in Africa (Figure 3).

All patients who acquired infection in Central America showed infection with P vivax. Seven P vivax cases were reported from Africa. The Africans more often reported a history of travel (52 of 70 Africans vs 8 of 17 non-Africans, P=0.03, chi square), while all except one Central American case-patient developed malaria after immigration to the United States.

Among 53 case-patients with available data on antimalarial pharmacologic prophylaxis, none was taken by 27 (51%) and what was taken was done so incompletely by 11 (21%). Such prophylaxis was used exclusively by Africans (26 of 45 Africans vs 0 of 8 non-Africans, P = 0.03, 1-tailed Fisher's exact test), consistent with the travel origin of African cases.

Treatment data were available for 72 (63%) case-patients. The most popular medications used for acute therapy were quinine (used among 20 of 37 [54%] P falciparum case-patients with data) and primaquine (used among 12 of 16 [75%] P vivax case-patients with data). Four of 16 (25%) P vivax case-patients with data were not given primaquine therapy. More than one medication was given to 51 case-patients (71%), while a single medication was employed with 19 (26%) case-patients, and two (3%) did not receive any pharmacologic treatment. Only one case-patient (a Cameroonian) reported a history of artemisinin-based combination therapy, administered in his home country.  


The incidence of malaria in the Southeastern United States was intertwined with slavery and economic conditions.1 As the price of agricultural products increased, farmers placed more importance on drainage for crops, the foci of mosquitoes diminished, and the incidence of malaria fell.2 Anophelism (the presence of mosquitoes) with its attendant surges in malarial cases occurred more frequently "in rural areas of valleys, coastal plains, and piedmont sections of the Southeastern states" (Figure 4) and in areas where poor housing and living conditions existed.2 These predisposing conditions may explain why Texas, one of the southern states where malaria had a strong presence, reached a toll of 25,000 cases per year by 1935. According to Dr. James Steele, most cases in Texas occurred in the border region because of a larger community of Central Americans. A map depicting the number of deaths due to malaria from 1938 through 1942 confirms his statement that most cases in Texas were concentrated in the border region2 (Figure 5).

Historically, poverty is not the only risk factor for malaria. Climactic changes are also very important. The seasonal predilection for late summer reported in this paper is also described in historical accounts. A description from 1876 includes the observation that most cases of malarial "chills" occur in August and September,11 a time of year when malaria was often referred to as "autumnal fevers."1  

Significant funding in control efforts for the prevention of malaria increased during World War I, but after the war investments in the area diminished and an increase in cases occurred.1 Again, control efforts restarted and malaria decreased.1,12 The decline in malaria cases to 2881 during 1949-1950 in Texas is attributable to a variety of control measures including, foremost, the reduction of foci for infection through drainage, larviciding, use of pyrethrum sprays, and the prescription of guanidine.1  

In our data, we see a surge in malaria cases in the early 1940s at the onset of World War II, which may have been a consequence of imported cases from returning soldiers and their relapses. During 1945 and 1946, many thousands of veterans returned to the United States carrying P vivax, which had been shown experimentally to be effectively transmitted by native US anopheles. Some fear existed that malaria could spread in the country, especially in the Southeast, where "anophelism still prevailed." Texas was one of 13 states participating in the National Malaria Eradication Program, which began in 1945.13 The program was headquartered in Atlanta (because of the higher rates of malaria in the South) and was a direct forerunner of the Centers for Disease Control and Prevention (CDC).14 The program focused on the use of DDT (an agent Dr Steele referred to as the "new boxer in the ring"), which radically finished off the endemicity of malaria. The data in this article show only sporadic cases reported in Texas after about 1952.

Nevertheless, our data revealed a number of travel-associated cases (625) from 1952 through 1959, long before the surges of modern intercontinental jet transport. As emphasized by Andrews et al, however, even in the states with the best records, introduced cases tend to be underreported, and these data may be a fraction of the actual number of cases.13

The rare autochthonous cases reported from Houston in the 1990s were 3 homeless patients exposed to anopheles at night in a region with a high number of immigrants.10 The recently reported cases in Houston tended to be among young (mean age, 32.8 years) persons who were more often male (men were almost twice as likely to be infected). These traits probably reflect the characteristics of immigrants or travelers.

The data in this paper reflect national trends, with 70.3% of cases reported to CDC in 2008 being from Africa and only 5.5% of cases from Central and South America combined. The higher percentage of Central Americans in these data reflect the patterns of migration, the proximity of Houston to Central America, and Houston's position as a travelers hub with daily flights to all major Central American cities.

Multiple studies show that the organism in most African cases speciates as P falciparum. The 81% of falciparum cases in this series was higher than the national average of 69%15, and this may reflect selective emigration to Houston from English-speaking areas of Central and Eastern Africa.

Very efficacious ways exist to prevent malaria,16 although adherence has been a problem historically.17 GeoSentinel data18 show that globally only 44.2% of travelers have a pretravel encounter with a health care provider, and CDC16 data show that nationally only 28.3% of travelers take prophylaxis; only a one-fifth of these complete it. While our data report a larger percentage taking prophylaxis (49%), only half of these claimed to have completed it.

The World Health Organization recommends artemisinin-based combination therapies as the best treatment option.19 Physicians in the United States have no easy access to artemisinin-based regimens that are not approved for marketing in this country by the Food and Drug Administration. In this series, no patient received artemisinin-based therapy in the United States, echoing the similar results of the local pediatric series.9 The hazards of monotherapy (carried out in this series among 26% of patients) in promoting antimalarial resistance are known.20    


Malaria in Houston evolved from a local highly endemic disease with surges late in the summer every year to one where most cases were associated with travel, except for occasional autochthonous cases. In the present, malaria is virtually imported exclusively and associated with immigration and travel. Current attempts at prevention require community education of high-risk immigrant and native African populations plus continued surveillance for local transmission.    


The authors thank the Research Division of the City of Houston Health Department for its contribution of data; Dr Jim Schuerman of the Texas Department of Health Services, Austin, Texas, for data; Dr Gloria Oramasionwu of Texas Children's Hospital for advice; and Dr James Steele (retired) for a historical perspective.   


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