Chapter 17
Amebiasis and Other Parasitic Diseases
Brigadier General Andre J. Ognibene, MC, USA, Colonel Ralph F. Wells, MC USA (Ret.), and Colonel O`Neill Barrett, Jr., MC, USA (Ret.)
Section I. Amebiasis
Brigadier General Andre J. Ognibene, MC, USA, and Colonel Ralph F. Wells, MC, USA (Ret)
HISTORY AND MILITARY SIGNIFICANCE
Amebiasis was unrecognized as a clinical entity among U.S. forces until the Philippine Insurrection. Although the British experienced significant amebic disease in the Gallipoli campaign (MD-PM4, p. 485), reporting in U.S. troops during World War I was limited: in a laboratory survey of 934 cases of dysentery, only 38 specimens were positive for amebas (MD-WW6, p.1101). With increased awareness, reporting of amebic diseases changed radically during World War II.
Official estimates are that approximately 1,261,000 man-days were lost because of diagnosed cases of amebiasis in the United States Armed Forces during World War II (TB MED). Amebic dysentery admission rates per 1,000 per annum for 1944-45 were 22.39 in the China-Burma-India theater (8,734 admissions), 5.63 in the Southwest Pacific (8,865 admissions), and 2.94 in the Central and South Pacific (2,393 admissions) (MD-PM4, p. 488). The admission rate of persons who were incidentally discovered to be asymptomatic carriers roughly paralleled that of persons with overt colitis in each of the above theaters. The crucial questions of actual carrier rate and prevalence of amebiasis in the indigenous populations were never answered.
Initial awareness of the disease in the United States was prompted by Giffin`s report (1913) which noted a 4.6-percent incidence of carriers in a series of studies at the Mayo Clinic. More recent estimates also indicate an average carrier rate of 5 percent (Brooke 1964).
The Chicago epidemic of 1933 demonstrated the importance of contaminated water as a source of infection (NIH Bull). Subsequent studies of water purification showed that cysts of Entamoeba histolytica are more resistant to chlorination than are fecal bacteria (Chang and Fair 1941).
The adverse environmental conditions under which military operations are conducted can reasonably be expected to increase the incidence of amebiasis.
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Large numbers of servicemen were exposed to infection abroad during World War I, World War II, and the Korean war. Public health authorities feared that returning infected troops would cause an increase in the incidence of disease in the United States (Juniper 1971). Studies on persons returning from combat theaters, however, failed to substantiate such fears (Brooke, Donaldson, and Brown 1954).
Precise data on the incidence of extra-intestinal manifestations of amebiasis were not generated during World War II, although concern about amebic abscess led to the definitive work of Klatskin and Friedman (1948) on abscess and specific emetine therapy. Conan (1948) and Murgatroyd and Kent (1948) independently reported on the effectiveness of chloroquine in the treatment of extra-intestinal amebiasis. The next major breakthrough in the treatment of hepatic abscess was use of metronidazole, introduced by Powell and coworkers (1966). While this drug was not approved by the Food and Drug Administration until the 1970`s, its effectiveness against both the intraluminal and tissue phases of the disease resulted in its use by many U.S. military physicians during the peak years of the Vietnam conflict (Everett 1974).
INCIDENCE AND EPIDEMIOLOGY
It is almost axiomatic that amebiasis is a worldwide problem with its most frequent clinical expression in the Tropics and decreasing frequency of occurrence in more temperate climates. In the Tropics, E. histolytica vies with shigellosis as the major cause of diagnosed dysentery while in temperate climates shigellosis is more prevalent. A report by Elsdon-Dew (1968) delineates global trends from 1946 to 1956 and will be of interest to readers desiring more specific epidemiological information.
All epidemiological data concerning the incidence of amebic disease must be relatively suspect since the data reported to any central agency, such as the World Health Organization, are no more accurate than the observations of the physician or parasitologist involved with the individual patient. The Armed Forces Epidemiological Board report (Gezon 1966) focuses specifically on this problem as it applied to experience in Vietnam. The problem is further complicated by the detection of quadrinucleate cysts of nonpathogenic amebas in the stool which may be erroneously reported as E. histolytica.
ETIOLOGY AND PATHOGENESIS
"Amebiasis" generally refers to a whole spectrum of diseases in which an ameba with tissue-invading capability, usually E. histolytica, colonizes a tissue, producing necrosis and abscess formation. In its most benign form, the infection may be clinically inapparent and will be recognized only because the patient is shedding cysts in his stool. Clinically apparent amebiasis is usually manifested by diarrhea with or without gross bleeding. Less commonly, the ameba may produce a variety of clinical syndromes including single or multiple hepatic abscesses, ameboma of the colon, acute appendicitis, and fistulas to the biliary
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tract, lung or pericardium, or even to the skin. Rarely, central nervous system involvement may occur. Dietschy (1974) reviewed the subject of amebiasis in depth, and this section draws extensively on his review.
All amebas belong to the phylum Protozoa, the class Rhizopoda, and the order Amoebida. Characteristically these organisms do not contain a cell wall and generally form pseudopodia by alternately shifting the cytosol from a gel to a sol phase. The order Amoebida may be divided further into those organisms which are principally free-living and those which are strictly parasitic.
The various genera of the family Endamoebidae generally are differentiated in terms of their morphologic characteristics, in particular the morphology of the nucleus on stained specimens. Several species of Endamoebidae occur in man, including Entamoeba histolytica, Entamoebacoli, Entamoeba gingivalis, Entamoeba polecki, Endolimax nana, Iodamoeba buetschlii, and Dientamoeba fragilis. All are lumen dwellers except E. gingivalis, and almost all except E. histolytica lack the ability to invade tissue.
All of the parasitic amebas have a similar life cycle, which begins for the host with the ingestion of the cyst. Little happens to the ingested cyst in the acid milieu of the stomach, but on entering the alkaline environment of the duodenum, dissolution of the cell wall and excystation follow. As a rule, the cytosol fragments into as many pieces as there are nuclei. The resulting structure is a metacystic trophozoite, which does not colonize the small intestine but passes rapidly to the colon. In the nonpathological strains, trophozoites phagocytize bacteria and other nutrients from the colonic contents. Under special circumstances, probably related to the bacterial flora of the gut, the trophozoite of E. histolytica is also capable of tissue invasion and active phagocytosis of cell components after dissolution of the cell membrane. In all species, the trophozoites reproduce within the luminal contents or colonic crypts by binary fission. The mature trophozoites are excreted in the stool only when a liquid or diarrheal stool is passed. During the process of solid stool formation, encystation occurs. As this occurs, the trophozoite undergoes loss of cytoplasmic vacuoles and condensation of the cytosol and cell membrane. In some species the nucleus reduplicates, so that cysts of E. histolytica in the precyst phase may form one, two, or four nuclei. The mature cyst is then excreted in the feces and enters the environment where it may persist for extended periods until ingested by another host (Hunter, Frye, and Swartzwelder 1966, pp. 269-308).
E. coli has a large trophozoite form, 20 to 30 i, in diameter, but its unique feature is a mature cyst usually containing eight nuclei. It may coexist with E. histolytica. It is a nonpathogen, and its chief importance is as an indicator of in gestion of fecally contaminated food. E. gingivalis is a parasite of the human mouth and is transmitted by direct oral contact or by droplet dissemination. E. polecki inhabits the colon of the monkey and the pig. One case of human disease, in a Peace Corps worker, has been reported (Levin and Armstrong 1970).
E. moshkovskii has been found in sewage containing human feces. Its pathogenicity is unknown. End. nana is a nonpathogen, although it may be occasionally detected in diarrheal stools. I. buetschlii may rarely cause tissue invasion with colitis or dissemination to the lung or brain while D. fragilis may cause
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nonspecific mucosal irritation, hypermotility, abdominal pain, and diarrhea.
While the pathogenicity of the above organisms is still undecided, there is little doubt that in man the vast majority of clinical disease is produced by E. histolytica because of its capacity for aggressive tissue invasion (fig. 71). However, it has become apparent in recent years that the conventional morphologic criteria for the identification of E. histolytica cysts are totally inadequate. Variation in cyst size is recognized; a large race and a small race have been identified (Hunter, Frye, and Swartzwelder 1966, p. 276). The small race is now classified as E. hartmanni and is of questionable pathogenicity.
Recent work (Goldman 1969) has demonstrated that even the group of amebas designated as large race E. histolytica are not homogenous. The Laredo type (Laredo, Huff, 403, Nelson`s, AG, and JA strains) has vastly different physical, cultural, and biochemical characteristics from pathogenic E. histolytica. The Laredo type can survive temperatures of 0° to 41°C, will grow in culture at temperatures as low as 10° C, and will survive in hypotonic media at a dilution of 1:64, as opposed to E. histolytica, which has a survival range of 20° to 43?C, a minimum temperature for growth in culture of approximately 30° C, and can survive only a 1:2 media dilution. The Laredo type will infect man but produces no disease; this is fortunate as it is consistently quite resistant to most antiamebic drugs. E. moshkovskii is another large strain nonpathogen which has the capacity to survive in low temperatures and in markedly hyposmotic incubation media. These strains-the Laredo type and E. moshkovskii-are mentioned only because of the possibility that asymptomatic carriers may not in fact be infected with E. histolytica but rather with one of these morphologically indistinguishable quadrinucleate strains analogous to the carrier state for E. coli..
The precise mechanism by which trophozoites attack and invade tissues is unknown (fig. 72). The notion that a toxic substance produced by the amebas lyses normal cells, thus initiating invasion, might well be challenged on the basis of research on the pathogenesis of the disease. In cell cultures, the amebas are surrounded by lysed cells while more distant cells remain healthy. Phase microscopy and electron microscopy have been employed to study what happens. In all cultures when a cell comes in contact with the plasmalemma of the amebas, there is an immediate change in the characteristics of the cell membrane. Cell organelles become more prominent, the cell shrinks, and soon blebs of cytosol extrude from the portion of the cell in contact with the amebas. The amebas then begin to engulf the damaged cell either piecemeal or entirely. The mechanism of the contact lysis has been studied by electron microscopy. The amebas have a "fuzzy layer" representing surface lysosomes. This fuzzy layer has numerous shallow depressions, in the center of which is found a tubular projection or "trigger." This trigger comes in contact with the cell under attack. When contact is made, the trigger ruptures, emitting a toxin (hydrolytic enzymes?) capable of dissolving the limiting membrane of the target cell. Phagocytosis then progresses by an unknown mechanism. To date, there are no comparative data on the presence or absence of the surface lysosomes in pathogenic versus nonpathogenic organisms. Clarification of this process remains a major challenge.
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FIGURE 72.-Trophozoites of Entamoeba histolytica invading intestinal wall.
CLINICAL FEATURES, COURSE, AND COMPLICATIONS
The colon is the primary target organ for infection with E. histolytica. The subsequent clinical course is contingent upon the degree of invasiveness of the parasite in that organ. While clinical amebiasis is usually characterized by a diarrheal syndrome, the spectrum of severity ranges from the asymptomatic cyst passer to the patient with extra-colonic invasion either by contiguous spread or hematogenous dissemination. Hepatic involvement with abscess formation is most common in the latter situation. For example, direct spread by fistula formation may occur from the liver to the pleural or peritoneal cavities, the tracheobronchial tree, the pericardium, the biliary tract, or the skin, while hematogenous spread may lead to amebic abscesses in the lung parenchyma, brain, spleen, or kidneys.
The Asymptomatic Cyst Passer
Many asymptomatic individuals have cysts of E. histolytica in their stools. It is not known whether this is a function of the host or a characteristic of the parasite itself. The roles of gut flora and diet have been studied extensively without achieving a definitive explanation. The majority of persons in this category are detected by population surveys or during the course of epidemiological studies. Some authors would classify patients with "irritable
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colon" symptoms and cysts in their stools as asymptomatic cyst passers if proctoscopy proved normal and trophozoites were absent (Curtis and Sleisenger 1973, pp. 1388-89; Hunter, Frye, and Swartzwelder 1966, p. 295).
Amebic Colitis
Clinical presentation of patients with amebic dysentery may run the gamut from a mild diarrheal disease to a fulminant process with severe systemic toxicity. Whatever the mechanism triggering tissue invasion, the process precedes the onset of clinical symptoms. The initial lesion seen at proctoscopy consists of a pinhead-size ulcer with hyperemic margins reaching only the muscularis mucosa. In some patients a more extensive superficial erosion is seen. This is followed by enlargement and penetration with an "inverted tack" appearance and overhanging edges. Aspirates, scrapings, or biopsy of these lesions will show numerous trophozoites. In many cases, the mucosa may be diffusely involved, mimicking nonspecific ulcerative colitis. The P.M.N. (polymorphonuclear neutrophil leukocyte) response is relatively less than one would expect and there is a corresponding reduction of P.M.N.`s on the fecal leukocyte smear.
Most primary intestinal lesions occur in the colon except for approximately 5 percent which occur in the lower ileum near the ileocecal valve. The ulcerations seem to be most common in the cecum, ascending colon, and the sigmoido rectal region. Sixty-one percent of patients will have multiple lesions scattered throughout the colon (Belding 1965, p.65).
The process may be acute with severe bloody diarrhea, volume depletion, and occasional local complications such as amebic appendicitis, perforation with pericolic abscess, or "toxic megacolon" clinically indistinguishable from ulcerative colitis. Other complications include ameboma or granuloma formation and strictures. It is particularly important that ameboma be distinguished from carcinoma to avoid unnecessary radical surgery. Colitis must be distinguished from idiopathic ulcerative colitis to preclude steroid therapy; this can be done by demonstration of invasive trophozoites. Some patients may experience a chronic colitis in which a persistent non bloody diarrhea may occur.
The therapy of acute amebic colitis was a source of confusion for the U.S. physician in Vietnam because of misleading claims about the efficacy of various regimens and because the need to address all possible sites (bowel lumen, intestinal wall, and liver) was overlooked. Powell (1971) summarized the action of available amebicides (table 74). Emetine was 30 to 50 percent effective, tetracycline 97 percent, and chloroquine 10 percent. At the beginning of the Vietnam war, most physicians were using a combination of all three drugs to achieve a complete therapeutic success, especially in severe cases. Soon after arriving in Vietnam, however, physicians questioned this therapeutic approach.
Carlin and Martin (1970) addressed the lack of uniformity in therapy and the question of whether chloroquine and/or emetine were needed in all cases. They were prompted by the report of Powell and coworkers (1966) on the efficacy of metronidazole to study its use in U.S. troops. Of 25 soldiers with amebic dysentery, almost all showed improvement within hours after their first dose of
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TABLE 74.-Site of action of amebicides used for acute amebic colitis in Vietnam
the drug, given 750 mg three times daily. By the fifth day, 50 percent could be discharged as asymptomatic; by the tenth day this figure had increased to 92 percent. Temperatures normalized and pain in the right upper quadrant decreased promptly in eight patients with suspected liver abscess; all became ambulatory by the seventh day and were transferred to Japan for hepatic scanning. Followup on four of these patients confirmed abscess, with subsequent resolution in three. The patient with a negative scan had presented with a flank mass, positive stool examination, and abnormal SGOT (serum glutamic-oxaloacetic transaminase) and BSP (Bromsulphalein). He was scanned 2 weeks later and had no evidence of abscess.
This study further emphasized the importance of early sigmoidoscopy and direct examination of rectal mucus by the physician. Of the study patients, 75 percent were diagnosed on admission by meticulous and direct examination of sigmoidoscopically collected material.
In the patient with an active colitis, one of the most definitive diagnostic procedures is the demonstration of motile trophozoites with ingested red blood cells in the liquid or diarrheal stool. Even more productive is the examination of wet preparation obtained at proctosigmoidoscopy by aspiration or scraping of ulcers. Iron hematoxylin staining will increase the yield of positive findings (Curtis and Sleisenger 1973, pp. 1388-89). When immediate laboratory support is not available, use of PVA (polyvinyl alcohol) as a slide fixative or as a preservative mixed with equal parts of stool will facilitate the task of the diagnostic laboratory. Schaudinn`s fixative is another useful vehicle allowing subsequent staining of a thin smear immersed in the solution. Rectal biopsy is a useful adjunct depending on available laboratory support.
Equipment and technical support to provide the necessary diagnostic capability were not available at the unit level in Vietnam; consequently, diagnosis of amebiasis was difficult in division-level medical service. Patients with diarrheal syndromes persisting beyond 48 hours, with accompanying fever or bloody diarrhea, required evacuation to a hospital facility for definitive study. Unsupervised antibiotic administration served only to hamper further diagnostic efforts and was discouraged.
Local Complications From Amebic Colitis
Acute perforation of the colon occurs in 1.5 percent of all cases, and in 4 to 19 percent of fatal cases. Autopsy incidence of perforation and peritonitis ranges from 29 to 74 percent (Belding 1965, p. 67). Perforation with pericolic abscess is
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shown in figure 73. Perforations are most common in the cecum and rectosigmoid area, and multiple perforations are frequent. Abdominal distention, fever, and ascites are associated with perforation. Diagnostic paracentesis may demonstrate trophozoites.
Amebic appendicitis is indistinguishable from conventional appendicitis. The differential diagnosis in a young soldier in Vietnam often posed significant difficulty. The only clue may be a prior history of diarrheal disease. If appropriate chemotherapy is not initiated, a fecal fistula, cutaneous amebiasis, or intra-abdominal abscess may occur. Patients may go on to develop mixed amebic and pyogenic abscesses of the liver with a cutaneous-hepatic-biliary fistula.
There may also be primary cutaneous involvement or involvement of the female genital tract. These problems were rarely seen among U.S. personnel in Vietnam.
Amebic Abscess of the Liver
Amebic liver abscess is the most serious complication of amebiasis and, if unrecognized, causes considerable mortality (fig.74). The diagnosis may be difficult because of the absence of a history of diarrhea and/or the inordinate delay between exposure and clinical presentation. Eighty to 85 percent of abscesses occur in the right lobe. Right upper quadrant pain, fever, chills, and weight loss are common features. Occasionally there may be point tenderness over the liver. Less commonly, the patient may present with a pleural effusion or cough or, in a left lobe abscess, with pericardial involvement. Jaundice is rarely seen. Stool studies are frequently negative, and the diagnosis is based on clinical assessment, liver scan, serologic testing, or, in some circumstances, diagnostic aspiration. Approximately 85 percent of patients will have radiographic abnormality on chest X-ray, including elevated right hemidiaphragm, loss of motility of the diaphragm, blunting of the costophrenic angle, atelectasis, and pleural effusion (Belding 1965, pp. 81-82).
Radioisotope capability was never established in Vietnam, although two significant studies of liver abscess were conducted on Vietnam returnees, one in Japan and one at Walter Reed Army Medical Center. The latter (Sheehy et al.1968) documented the resolution time as determined by serial liver scans. A defect persisted an average of 4.3 months. Rarely a "cold spot" was demonstrable as long as 1 year after "definitive" treatment (fig.75). In our opinion, persistent pain after abscess treatment was caused by either an incompletely resolved abscess or adhesions between Glisson`s capsule and the parietal peritoneum analogous to the Fitz-Hugh-Curtis syndrome seen after gonorrhea infection.
The Japan study (Levin 1969) summarized experience, from 15 July 1968 to 3 April 1969, with 42 patients with hepatic abscess who were evacuated to Camp Zama. The presenting complaints of 31 of the patients were as follows:
Fever - 13 Anorexia - 2
Right upper quadrant abdominal pain - 10 Right shoulder pain - 1
Diarrhea - 5
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The clinical findings are shown in table 75. The triad of fever, anorexia, and weight loss was almost universal, with right upper quadrant pain characteristically adding to the presentation. Laboratory findings are given in table 76. Leukocytosis and an abnormal prothrombin time were almost always present. Massive hepatomegaly was unusual (table 77). More than half the patients had minimal hepatic enlargement or normal size livers upon physical examination.
There were 52 abscesses identified in the 42 patients, located as follows (lobe was not determined in two cases; abscess was seen only on the lateral view):
Lobe (right) - 47 Inferior third of liver - 16
Lobe (left) - 2 Anterior (lateral scan) - 20
Lobe (right and left) - 1 Central ( lateral scan) - 10
Superior third of liver - 27 Posterior (lateral scan) - 22
Mid third of liver - 9
The estimated sizes of the 52 abscesses were as follows:
17-150 cm3 - 23 451-600 cm3 - 3
151-300 cm3 - 11 Over 601 cm3 - 4
301-450 cm3 -6
The four largest abscesses measured 746, 1,028, 1,540, and 1,690 cm3. Five abscesses were not visualized on the anterior view, and therefore were measured in cm2.
Of the 42 patients, 6 required needle aspiration or surgical drainage because of failure to respond to drug therapy or because of increase in abscess size. All patients were treated with emetine, chloroquine, Diodoquin, and tetracycline. After April 1969, metronidazole was used extensively; however, definitive analysis of its effectiveness in hepatic abscess was incomplete at the time of cessation of hostilities.
Everett (1974) did review 12 patients with amebic liver abscesses acquired in Vietnam who were treated solely with metronidazole. Neither duration of illness nor size of the abscess had predictable correlation with response to therapy or healing rate. Metronidazole in doses of 750 mg three times a day for 10 days was effective in this series.?
Serodiagnosis
A number of serologic techniques have been used in the past for diagnosis when stools were negative or other laboratory support questionable. During the
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Vietnam conflict, the Moan precipitin test became obsolete and was replaced by several new techniques. The IHA (indirect hemagglutination) test introduced by Lewis and Kessel (1961) and standardized by Milgram, Healy, and Kagan (1966) more closely approaches a definitive serologic test for amebiasis than any other previously available. A positive IHA response is seen in 85 to 96 percent of patients with hepatic amebiasis (100 percent positivity has been found in some small series) and in 82 to 95 percent of patients with invasive colonic disease (Juniper et al. 1972; Milgram, Healy, and Kagan 1966; Kessel et al. 1965). About 1 percent false positive reaction may be detected in the general population. The
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two major drawbacks of the IHA are the lack of general availability and persistent positivity in treated patients. The test, however, was not available in Vietnam and was available in the continental United States only through the Center for Disease Control. As a result, it served only to confirm a diagnosis made by other means.
A combination of microimmunoelectrophoresis pattern analysis and IHA titer level used in a South African study (Krupp and Powell 1971) has helped to provide differentiation between active infection and persistent antibody positivity after treatment. There was little U.S. experience with this combination of techniques. The SAFA (soluble antigen fluorescent antibody) test devised by Sadun was readily available to military physicians, and recently a reliable latex fixation test kit yielding results similar to the IHA has become available. The CF (complement fixation) test at titers of 1:16 or above strongly suggests active disease and is useful in assessing the clinical significance of the positive IHA or latex fixation (Healy and Cahill 1971). In Vietnam, however, serological tests did not replace skilled clinical judgment and therapy could not await serological confirmation.
Treatment
Appropriate guidelines for the management of various types of E. histolytica infections were reported toward the close of the Vietnam conflict in The Medical Letter (table 78). Metronidazole was established as the drug of choice for both intraluminal and extraluminal amebiasis. As mentioned earlier, some controversy surrounded the treatment of amebiasis during the Vietnam war because many physicians wished to use this drug rather than conventional chemotherapeutic regimens although it was not yet FDA-approved for such therapy. The drug was used in Vietnam for amebiasis and giardiasis, but results of its efficacy were not extensively tabulated.
While a number of advances were made in the study of amebiasis, the only one to have a significant impact in Vietnam per se was the use of metronidazole. Neither nuclear medicine capability nor contemporary serodiagnostic methods were ever available there. In future conflicts in a tropical area, nuclear medicine capability and clinical laboratory support must be made readily available to preclude either unnecessary evacuation of personnel or delay in diagnosis.
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TABLE 78.-Treatment schedule for amebic disorders caused by Entamoeba histolytica
Section II. Other Parasitic Diseases
Colonel O`Neill Barrett, Jr., MC, USA (Ret)
INCIDENCE
Although a variety of parasites infested the Vietnamese civilian population, they were not a significant problem for American troops. Stool examinations of 235 civilians surveyed in Binh Duc village of Dinh Tuong Province in the Mekong Delta in 1968 showed 78 percent to be infested with roundworms (Ascaris lumbricoides); 35 of those infested also had hookworm (Necator americanus) (Poffenbarger 1972). In a prospective study of 500 American returnees from Vietnam, Sheehy and coworkers (1965) found that only 15 percent harbored intestinal parasites. Table 79 gives a breakdown of parasites found in 75 returnees.
HOOKWORM
Hookworm, the most common intestinal parasite seen in American troops in
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TABLE 79.-Incidence of intestinal parasites in 75 American servicemen returning from Vietnam
Vietnam, frequently caused troublesome symptoms and occasionally morbidity. Isolated outbreaks of infestation were documented; in one such outbreak, 39 men from a unit of the 1st Cavalry Division were hospitalized with severe hookworm gastroenteritis (Vandevelde 1966). It became clear that one need not go barefoot to become infested with hookworm in Vietnam; mud or muddy water seeping through the air vents or eyelets of boots, and other forms of earth contact, such as digging foxholes and leaning against parapets, were all sources of infestation (Sheehy 1968, p.108).
A variety of symptoms can be produced by hookworm, especially in previously unexposed persons who acquire a heavy infestation with larvae. These include "ground itch" and "foxhole cough," as well as an acute duodenitis that clinically mimics peptic ulcer disease (Rogers and Dammin 1946).
The only detailed clinical study of hookworm infestation in American troops was performed by Levine and Sheehy (1966), who studied 11 patients admitted to the 3d Field Hospital, Saigon, with probable diagnoses of peptic ulcer. Gastrointestinal symptoms were always a prominent part of the clinical syndrome of these patients and apparently began 6 to 18 weeks after exposure. In some instances, the patients presented with an acute attack of abdominal pain, nausea, vomiting, and diarrhea, while in others, the symptoms were chronic and were associated with diarrhea and weight loss. Pain was the most prominent symptom and was usually epigastric. However, in contrast to the pain in peptic ulcer, it was aggravated rather than relieved by ingestion of food. Eosinophilia was an important laboratory finding; of the 11 patients, 9 had an absolute eosinophilia (greater than 500 per mm3), with eosinophils ranging from 7 to 38 percent of the total count. Roentgenologic changes in the gastrointestinal tract were common and included a "deficiency pattern" characterized by excessive peristaltic activity, segmental contractions of the small bowel, and distortion of the mucosal pattern. Improvement in the roentgen manifestations occurred promptly after therapy was begun.
The syndrome of abdominal pain simulating peptic ulcer but made worse by food, gastrointestinal roentgenograms which do not show an ulcer crater, and eosinophilia, especially in tropical areas, suggests hookworm infestation.
FILARIASIS
The problem of filariasis in U.S. troops has been recognized since World
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War II. In the Central and South Pacific, there were large outbreaks of filariasis among military personnel. Wartman and King (1944) reported their experience with 268 Americans who developed acute filariasis with fever, lymphangitis, lymphedema, and scrotal inflammation, some of them as early as 3 months after arrival in the endemic areas. The average patient remained in the hospital for 16 days. When 25 of the patients were reevaluated in a follow up study, it was found that most continued to have clinical attacks during the 16 years they had been out of the South Pacific (Trent 1963).
Filariasis was shown to be endemic in North Vietnam in 1954 (Mille 1954). Earlier suggestions of filariasis caused by Wuchereria bancrofti in South Vietnam, especially in the area around An Loc, northwest of Saigon, were confirmed by a U.S. Army survey team in 1967. Prevalence studies showed evidence of infection in up to 22 percent of Montagnard tribespeople, and 15.2 percent of 112 servicemen on field duty in the endemic area had filarial antibodies as determined by the soluble antigen fluorescent antibody test (Colwell et al. 1970). Microfilaremia, however, was rare (Beaver 1970). This, along with other data, supports the contention that the syndrome of "tropical eosinophilia" is caused by human or animal filariae, or both. The presence of antifilarial antibodies, marked eosinophilia, and dramatic response to diethylcarbamazine citrate, even in the absence of microfilaremia, lend credence to this hypothesis. Although only one clinically apparent case of filariasis in an American serviceman in Vietnam has been reported (Pittman 1972), cases of so-called tropical eosinophilia or otherwise unexplained eosinophilia in an individual who has been in an endemic area should raise the possibility of filariasis.
OTHER PARASITES
Strongyloides stercoralis parasites cause damage to the intestinal mucosa and, in cases of heavy infestation, produce malabsorption. Neither strongyloidosis nor ascariasis was an important cause of morbidity in American troops, but serious complications have been associated with both (Sheehy 1968, p.108). While Balantidium coli infection is known to occur throughout Southeast Asia, there has been only one documented case in an American serviceman returning from Vietnam (Lerman, Hall, and Barrett 1970).
Human schistosomiasis was not demonstrated in Vietnam, a fortunate circumstance in view of extensive military operations in watery terrain. The liver fluke, Clonorchis sinensis, was a serious problem for Vietnamese troops but was never reported in Americans. Other tissue flukes were known to occur in Vietnam, including Paragonimus westermani and Fasciolopsis buski,but were never observed in U.S. troops.?
TREATMENT
Because of the potential and real problem of parasitic infestations in American troops and the lack of previous experience among military physicians in treating them, once yearly the USARV (U.S. Army, Vietnam) medical consult-
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ant published an internal medicine sourcebook outlining therapy for the wide variety of diseases seen in Vietnam. The treatment schedule for those parasitic infestations, published in 1971, is shown in table 80.
TABLE 80.-Treatment schedule for parasitic infestations in Vietnam, 1971
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TABLE 80.-Treatnment schedule for parasitic infestations in Vietnam, 1971-Continued
REFERENCES
Amebiasis, Department of the Army Technical Bulletin (Medical). See TB MED.
Beaver, P. C. 1970. Filariasis without microfilaremia. Am. J. Trop. Med. 19:181-89.
Belding, D. L. 1965. Textbook of parasitology. 3d ed. New York: Appleton-Century-Crofts.
Brooke, M.M. 1964.Epidemiology of amebiasis in the U.S. JA.M.A. 188: 519-21.
Brooke, M. M.; Donaldson, A. W.; and Brown, E. 1954. An amebiasis survey in a Veterans Administration Hospital, Chamblee, Georgia, with comparison of technics. Am. J. Trop. Med.3: 615-20.
Carlin, A. W., and Martin, R. L.1970. Flagylin the treatment of amebiasis. USARVM. Bull. (USARV Pam 40-23),Sept.-Oct., pp. 36-42. Copy in Joint Medical Library, Office of the Surgeons General.
Chang, S. L., and Fair, G. M.1941. Viability and destruction of the cysts of Endamoeba histolytica J. Am. Water Works A. 33:1705-15.
Colwell, E. J.; Armstrong, D. R.; Brown, J.D.; Duxbury, R. E.; Sadun, E. H.; and Legters, L. J.1970. Epidemiologic and serologic investigations of filariasis in indigenous populations and American soldiers in South Vietnam. Am. J. Trop. Med. 19: 227-81.
Communicable diseases transmitted chiefly through respiratory and alimentary tracts, Preventive Medicine in World War II. See MD-PM4.
Conan, N. J., Jr. 1948. Chloroquine in amebiasis. Am. J. Trop. Med. 28: 107-10.
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