5
LEVELS OF ASSOCIATION BETWEEN SELECT DISEASES AND LONG-TERM ADVERSE HEALTH OUTCOMES

Only 10% of the roughly 90 infectious diseases endemic in southwest and south-central Asia are likely to pose a long-term health risk to exposed US military personnel. As noted in Chapter 3, the long-term adverse health outcomes of most diseases endemic in the region would usually become apparent during or immediately after the acute illness, and many of the health outcomes are rare. However, nine of the infectious diseases meet the inclusion criteria outlined in Box 5.1 and discussed in Chapter 2. Those nine diseases and their associated long-term adverse health outcomes are the subject of this chapter (Table 5.1).

Following the paradigm of past Institute of Medicine Committees on Gulf War and Health, the committee determined the strength of association between each infection1 and specific long-term adverse health outcomes in humans. For every health outcome discussed in this chapter, there is limited or suggestive evidence of an association, sufficient evidence of an association, or sufficient evidence of a causal relationship with the infectious disease. Several delayed long-term adverse health outcomes of the nine diseases are listed in Chapter 3 but not reviewed here; the committee determined that there is inadequate or insufficient evidence of an association between these health outcomes and the infectious diseases. To reach its conclusions, the committee assessed the available evidence published in the biomedical literature about the long-term adverse outcomes of the diseases on human health.

BOX 5.1

Inclusion Criteria

The committee used these questions to evaluate the dozens of infectious diseases endemic in southwest and south-central Asia or commonly found among troops in wartime (Table 2.1). If the answer to every question was yes, a disease met the criteria for in-depth evaluation in this chapter.

  1. Was the infection or disease diagnosed in US troops in appropriate temporal relationship to deployment to the Gulf War, Operation Enduring Freedom, or Operation Iraqi Freedom, given the natural history of the disease?

  2. Is the risk of contracting the disease during deployment in southwest or south-central Asia equal to or greater than the risk of contracting it in the United States?

  3. Does the disease have a known or suspected long-term adverse health outcome?

  4. Would there be a delay between the infection or the end of the acute illness and the onset of the long-term adverse health outcome?

1

In this context, the term infection refers to a primary infection that leads to disease.



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Gulf War and Health: Volume 5. Infectious Diseases 5 LEVELS OF ASSOCIATION BETWEEN SELECT DISEASES AND LONG-TERM ADVERSE HEALTH OUTCOMES Only 10% of the roughly 90 infectious diseases endemic in southwest and south-central Asia are likely to pose a long-term health risk to exposed US military personnel. As noted in Chapter 3, the long-term adverse health outcomes of most diseases endemic in the region would usually become apparent during or immediately after the acute illness, and many of the health outcomes are rare. However, nine of the infectious diseases meet the inclusion criteria outlined in Box 5.1 and discussed in Chapter 2. Those nine diseases and their associated long-term adverse health outcomes are the subject of this chapter (Table 5.1). Following the paradigm of past Institute of Medicine Committees on Gulf War and Health, the committee determined the strength of association between each infection1 and specific long-term adverse health outcomes in humans. For every health outcome discussed in this chapter, there is limited or suggestive evidence of an association, sufficient evidence of an association, or sufficient evidence of a causal relationship with the infectious disease. Several delayed long-term adverse health outcomes of the nine diseases are listed in Chapter 3 but not reviewed here; the committee determined that there is inadequate or insufficient evidence of an association between these health outcomes and the infectious diseases. To reach its conclusions, the committee assessed the available evidence published in the biomedical literature about the long-term adverse outcomes of the diseases on human health. BOX 5.1 Inclusion Criteria The committee used these questions to evaluate the dozens of infectious diseases endemic in southwest and south-central Asia or commonly found among troops in wartime (Table 2.1). If the answer to every question was yes, a disease met the criteria for in-depth evaluation in this chapter. Was the infection or disease diagnosed in US troops in appropriate temporal relationship to deployment to the Gulf War, Operation Enduring Freedom, or Operation Iraqi Freedom, given the natural history of the disease? Is the risk of contracting the disease during deployment in southwest or south-central Asia equal to or greater than the risk of contracting it in the United States? Does the disease have a known or suspected long-term adverse health outcome? Would there be a delay between the infection or the end of the acute illness and the onset of the long-term adverse health outcome? 1 In this context, the term infection refers to a primary infection that leads to disease.

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Gulf War and Health: Volume 5. Infectious Diseases TABLE 5.1 The Nine Infectious Diseases Studied for Strength of Association with Specific Long-Term Adverse Health Outcomes Infectious Disease Long-Term Adverse Health Outcomes Evaluated for Strength of Association Brucellosis Arthritis Cardiovascular system infections Ophthalmologic manifestations Genito-urinary tract manifestations Hepatic abnormalities Neurologic manifestations Respiratory system infections Other symptoms (fatigue, inattention, amnesia, depression) Campylobacter infection Guillain-Barré syndrome Reactive arthritis Uveitis Leishmaniasis Delayed presentation of visceral leishmaniasis (VL)a Reactivation of VL in the context of future immunosuppression Post-kala-azar dermal leishmaniasis Malaria Clinical relapse Late presentation or recrudescence of disease Hematologic manifestations Ophthalmologic manifestations Nephrologic disease Neurologic and neuropsychiatric disease Coxiella burnetii infection (Q fever) Chronic hepatitis Endocarditis Osteomyelitis Post-Q fever fatigue syndrome Vascular infection Salmonella (nontyphoid) infection Reactive arthritis Shigella infection Hemolytic uremic syndrome Reactive arthritis Tuberculosisb Activation of latent tuberculosis infection Late manifestations of pulmonary and extrapulmonary tuberculosis West Nile virus infectionc Persistent deficits in cognition, movement, and daily functioning a Viscerotropic leishmaniasis is considered a subset of VL for the purposes of this discussion. b Tuberculosis (TB) does not meet inclusion criterion 1 (Box 5.1), because there have been no published reports of military personnel who developed active TB while deployed to the Gulf War, Operation Enduring Freedom (OEF), or Operation Iraqi Freedom (OIF). However, in a presentation to the committee, Kilpatrick (2005) indicated that 2.5% of military personnel deployed to OEF and OIF and given predeployment and postdeployment skin tests for TB seroconverted during their deployment; that is, they acquired new TB infections. Immunocompetent people who are infected with TB have a 10% lifetime risk of developing active TB; this risk increases dramatically in people who become immunosuppressed. Therefore, the committee decided to evaluate TB in depth. c West Nile virus infection does not meet inclusion criterion 4 (Box 5.1), because its health outcomes usually are manifested at the time of the acute illness. However, dramatic changes in the epidemiology of West Nile virus infection since the middle 1990s led the committee to decide to review it in depth. This chapter contains nine sections, with similar formats: one for each disease. Each begins with an introduction to the disease and its etiologic agent, which is followed by a brief description of the acute illness. Then, a summary of diagnostic criteria and methods and of treatment protocols is presented. Each section ends with an evidence-based discussion of the infection’s known long-term adverse health outcomes and their pathogenesis; this discussion is

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Gulf War and Health: Volume 5. Infectious Diseases the basis of the committee’s conclusions about the strength of association between the primary infection and each long-term adverse health outcome. DIARRHEAL DISEASES: CAMPYLOBACTER, NON-TYPHOID SALMONELLA, AND SHIGELLA INFECTIONS Among the many pathogens known to have caused diarrheal disease among US troops deployed to the Gulf War, Operation Enduring Freedom (OEF), or Operation Iraqi Freedom (OIF), three merit an examination of their potential long-term, adverse outcomes to veterans’ health: Campylobacter, Shigella, and Salmonella. Campylobacter Infection Campylobacter infections are common causes of acute diarrheal illnesses in humans globally (Blaser 2005). The committee examined three potential long-term adverse health outcomes of Campylobacter infection: Guillain-Barré syndrome, reactive arthritis, and uveitis. The most common pathogenic Campylobacter species is C. jejuni, but disease may also be caused by other species, especially C. coli, C. upsaliensis, C. lari, and C. fetus. The typical illness is acute diarrheal disease lasting 2-5 days accompanied by abdominal pain and fever. The illness responds well to antibiotic treatment but often is self-limited. Campylobacter occasionally causes an acute systemic infection. Transmission of Campylobacter Campylobacter species (spp.) infect humans most often through contaminated food or water. Drinking untreated water is a major risk factor for both sporadic and epidemic campylobacteriosis (Allos 2001; Blaser 2005). Foodborne infections occur chiefly after the consumption of improperly heated foods of animal origin; common vehicles include unpasteurized milk and undercooked chicken. Among wild and domesticated animals, Campylobacter spp. may be normal flora or pathogens (Blaser 2005). Rarely, the bacteria are transmitted by person-to-person contact; this occurs chiefly from the handling of feces of incontinent people, such as infants, who are infected. People suffering from an enteric illness may be infected with two or more bacterial, viral, protozoan, or helminthic pathogens. Some laboratory analyses of stool specimens from deployed troops who had a diagnosis of diarrheal illness found dual infections in a subset of patients, as described in Chapter 4. Endemicity in Southwest and South-Central Asia Campylobacter is a common cause of acute diarrhea in southwest and south-central Asia (Wilson 1991). In the United States, the bacteria frequently instigate both sporadic diarrhea and outbreaks (Wilson 1991). Acute Illness Patients with Campylobacter infections often present with a short prodrome of symptoms consisting chiefly of headache, myalgias, back pain, and fever. Within 24 hours, the illness centers on the gastrointestinal tract, producing abdominal pain and diarrhea (either may come

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Gulf War and Health: Volume 5. Infectious Diseases first). Common characteristics of the abdominal pain are unlocalized cramping that may be so severe as to mimic acute appendicitis; however, diarrhea predominates over abdominal pain in most patients. On the first day of diarrheal illness, the patient usually has four to 20 loose stools, and 25% of them may contain visible blood. Laboratory examination of stool specimens usually reveals gross or microscopic blood in all and leukocytes in 70%. Fever continues from the prodrome and persists for 24-48 hours. Symptoms usually begin to recede after 48 hours and resolve during the next few days. In rare cases, the illness may last longer. In the absence of antibiotic treatment, relapse occurs in about 20% of cases; relapses are usually milder than the initial episodes. Some people with Campylobacter infections are bacteremic (Mandell et al. 2005); this condition represents either a primary bacteremia or, rarely, the seeding of a distant organ (Blaser et al. 1986). Diagnosis During and After Acute Illness Diagnosis of the acute illness is based on culture of feces and, rarely, of blood. Culture-based tests even in the acute phase can have false-negative results, especially in infection by non-jejuni species, because Campylobacter spp. are difficult to grow in culture. Alternatively, the bacteria can be detected with polymerase-chain-reaction (PCR) assay of genetic material from stool specimens. Antibody testing, which is not commercially available, is less reliable because of the diversity of Campylobacter strains, the time required for a response to occur, and differences in magnitudes of responses among hosts. Infected people shed Campylobacter in stool for a mean of 2-3 weeks after the onset of symptoms; virtually no immunocompetent hosts are still shedding the organism after 8 weeks (Karmali and Fleming 1979; Svedhem and Kaijser 1980; Taylor et al. 1988). Thus, a culture or PCR test conducted more than 2 months after an acute episode of Campylobacter enteric disease would rarely be positive. After 2 months have elapsed, there is no reliable diagnostic test for exposure to Campylobacter in people who manifest diseases that could be late adverse health outcomes of a Campylobacter infection. Treatment of Acute Illness Fluid and electrolyte replacement is the treatment of choice for diarrheal illnesses. In patients who are still symptomatic at the time of diagnosis, antimicrobial treatment is recommended, particularly with fluoroquinolones and macrolides. Clinicians should be cognizant of Campylobacter’s growing resistance to those antimicrobials; the degree of resistance will reflect the use of antimicrobials in animal farming and in the local human population. Long-Term Adverse Health Outcomes of Campylobacter Infection On occasion, infection by Campylobacter spp. leads to long-term adverse health outcomes. The most serious health outcome associated with campylobacteriosis is Guillain-Barré syndrome (GBS). Reactive arthritis appears to occur after campylobacteriosis at a frequency greater than the background frequency. There is some evidence that uveitis is associated with Campylobacter infection. Guillain-Barré Syndrome The first report of an association between Campylobacter jejuni infection and GBS was published in 1982 (Rhodes and Tattersfield 1982). Numerous scientists have since investigated

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Gulf War and Health: Volume 5. Infectious Diseases the relationship between the two diseases and have published more than 200 reports in peer-reviewed journals. By the year 2000, those investigations had established that infection by C. jejuni causes about 30% of all cases of GBS (Allos 1997; Dingle et al. 2001; McCarthy and Giesecke 2001; Nachamkin 2002; Nachamkin et al. 1998; Nachamkin et al. 2001; Sinha et al. 2004; Tam et al. 2003). A number of other infectious diseases are also associated with GBS. GBS is a severe acute neurologic disease characterized by ascending paralysis with involvement of motor neurons and sometimes sensory neurons (Rhodes and Tattersfield 1982). Developing over a period of days, the symptoms of GBS may lead to paralysis of the respiratory muscles and death; however, with rapid supportive care, the fatality rate has been reduced from more than 10% to less than 5%. Between 10 and 20% of affected persons have permanent neurologic deficits, such as persistent muscle weakness and contractures. Most patients with GBS require hospitalization, and more than 20% require ventilatory support at some time during their illness. Recommended treatment should be started immediately and may include plasmapheresis and intravenous administration of immunoglobulins. Approximately 0.01-0.03% of US patients who suffer acute gastrointestinal disease due to C. jejuni will develop GBS (Allos 1997; Tauxe and Blake 1992). The risk of developing GBS during the 2 months after a symptomatic episode of C. jejuni infection is about 100 times greater than the risk in the general population (McCarthy and Giesecke 2001). The symptoms of GBS usually are manifested 7-28 days after the onset of gastrointestinal symptoms (Allos 1997; McCarthy and Giesecke 2001). There is no association between the severity of C. jejuni-induced gastrointestinal illness and the risk of developing GBS (Allos 2001). Rigorous serologic and culture studies have found and validated evidence of recent infection by C. jejuni in high percentages of patients with GBS. Several studies, including at least two case-control studies, showed that GBS patients were more likely than controls to have increased titers of antibodies to C. jejuni (Liu et al. 2003; Mishu et al. 1993). They demonstrated important trends and associations in populations but are neither standardized nor sufficiently accurate to be used for conclusive diagnosis in an individual patient. In another line of inquiry, seven independent studies found that 8-50% (mean, 30%) of stool specimens obtained from patients with GBS at the onset of symptoms were culture-positive for C. jejuni (Enders et al. 1993; Gruenewald et al. 1991; Hariharan et al. 1996; Kuroki et al. 1993; Rees et al. 1995; Ropper 1988; Speed et al. 1984). A positive culture is sufficient for diagnosis of Campylobacter-induced GBS but may be falsely negative, depending on the accuracy of the cultural procedures used, timing after symptom onset, clinical status, and antibiotic use. There are several types of GBS, including acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and Miller-Fisher syndrome (MFS). Antecedent Campylobacter infections have been linked with AMAN and MFS (Dingle et al. 2001; Kuwabara et al. 2004; Nachamkin et al. 1998); their association with AIDP is controversial (Kuwabara et al. 2004; Nachamkin et al. 1998). Molecular mimicry is believed to play a role in the nerve damage that occurs in Campylobacter-associated GBS (Nachamkin et al. 1998). Although the mechanism is unknown, some molecular structures on the surface of particular strains of Campylobacter appear to mimic either the glycolipids of peripheral nerves or specific proteins found in myelin (Allos 2001). The committee concludes that there is sufficient evidence of an association between Campylobacter jejuni infection and GBS, if the GBS is manifested within 2 months of the infection.

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Gulf War and Health: Volume 5. Infectious Diseases Reactive Arthritis Reactive arthritis (ReA), an acute nonpurulent form of arthritis, is a complication of many infectious diseases that affect parts of the body distinct from those involved in the acute illness (Yu and Kuipers 2003). The disease chiefly follows urogenital or diarrheal infections by multiple etiologic agents, including Campylobacter. ReA that occurs after an episode of campylobacteriosis usually is manifested within several weeks of the acute gastrointestinal illness (Blaser 2000). The clinical manifestations ReA range from isolated transient monoarthritis to severe multisystem disease. Although it can be highly inflammatory and severe, ReA usually is moderate in intensity. Patients often manifest such constitutional symptoms as fatigue, malaise, fever, and weight loss. The arthritis typically is asymmetric and additive, with new joints becoming involved over days or weeks. Joints of the lower extremities suffer most. Tendinitis is common, as are urogenital, ocular, and mucocutaneous lesions. Rarely, ReA is associated with aortic insufficiency and cardiac conduction abnormalities. Reiter’s syndrome—the triad of arthritis, urethritis, and conjunctivitis—makes up just one portion of the ReA spectrum and is more closely associated with Shigella and Chlamydia trachomatis infections than with Campylobacter. ReA following infections by various agents occurs most often, although not exclusively, in people who have the gene that encodes a histocompatibility antigen called HLA-B27. Between 30% and 85% of ReA patients have the HLA-B27 gene. However, only 8% of healthy people have the HLA-B27 gene, and only about 20% of them will develop ReA if they contract the triggering infections (NIH 2002). People who are 18-40 years old are at greatest risk for ReA. Men and women are equally likely to contract ReA from enterically-acquired infections; in contrast, ReA from sexually-acquired infections predominantly affects men. Long-term followup studies of patients who have ReA suggest that some joint symptoms persist for months in 10-60% of cases and that acute symptoms commonly recur (Hannu et al. 2004a; Hannu et al. 2002; Rees et al. 2004). Up to 25% of affected people must change or curtail their work because of joint symptoms. The symptoms of ReA usually last 1-21 weeks and occasionally up to a year (Skirrow and Blaser 2002). Symptoms that persist beyond a year tend to be mild and nondeforming. ReA is a clinical diagnosis, but the finding of HLA-B27 positivity is helpful. Treatment is symptomatic and uses primarily anti-inflammatory agents, including nonsteriodal anti-inflammatory agents, especially indomethacin. Population-based studies have provided the most convincing evidence of an association between Campylobacter infection and ReA. Two such studies found that 7% and 1.8% of patients with laboratory-confirmed Campylobacter infection later developed ReA (Hannu et al. 2002; Rees et al. 2004). They validated the results of three independently conducted rheumatologic surveys administered after distinct outbreaks of Campylobacter infection (Bremell et al. 1991; Eastmond et al. 1983; Hannu et al. 2004a). The surveys found that 0.7-2.6% of adults infected with Campylobacter later developed ReA. The scientific literature also contains reports of at least 40 sporadic cases of ReA associated with Campylobacter infection (Hannu et al. 2002). The disparate geographic locations of the studies—including Finland and California—indicate that the association of Campylobacter with ReA is a general, not local, phenomenon. The pathogenesis of bacteria-induced ReA is poorly understood. Campylobacter organisms invade such host cells as monocytes and dendritic cells, which transport the bacteria

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Gulf War and Health: Volume 5. Infectious Diseases through the bloodstream to multiple locations, including joints (Yu and Kuipers 2003). How Campylobacter and other ReA-causing bacteria survive persistently in joint cells remains unknown, as does the viability of Campylobacter organisms in those cells. Yu and Kuipers (2003) present a plausible hypothesis for the mechanism by which Campylobacter organisms induce joint-specific inflammation: that macrophages present antigenic peptides to CD8+ T lymphocytes through histocompatibility antigen HLA-B27. The T-cell receptor of CD8+ T lymphocytes is specific for both foreign and self peptides carried by HLA-B27. The process may activate CD8+ T lymphocytes and produce the initial inflammatory response. The mechanism of sustained inflammatory response is unknown. Despite the ambiguous pathogenesis of postinfection ReA, the weight of epidemiologic evidence convincingly illustrates that a small percentage of people infected by Campylobacter spp. later develop ReA. The committee concludes that there is sufficient evidence of an association between Campylobacter infection and reactive arthritis (ReA), if the ReA is manifested within 3 months of the infection. Most cases of ReA are manifested within a month of the infection. Uveitis Uveitis is an inflammation inside the eye that affects the uvea. Known causes of uveitis include autoimmune disorders, infection, and exposure to toxins (MedlinePlus Medical Encyclopedia 2006). In many cases, the cause is unknown. Three case reports describe uveitis after C. jejuni infection (Hannu et al. 2004b; Howard et al. 1987; Lever et al. 1984). The first report involves one of 350 patients who contracted C. jejuni infection in an outbreak in Finland in August 2000 (Hannu et al. 2004b). The subject of the report, a 72-year-old woman who had gastritis, developed pain and mucopurulent exudation in her left eye without marked redness after the C. jejuni outbreak. Although C. jejuni infection was not confirmed with a stool culture, it was “epidemiologically highly probable” that her prior gastrointestinal symptoms were caused by C. jejuni (Hannu et al. 2004b). About 3 weeks after the acute illness, the woman sought medical attention for the eye symptoms, and mild acute anterior uveitis was diagnosed. An HLA-B27 antigen test was negative. She was treated with local corticosteroid drops and corticosteroid-antibiotic ointment. The condition resolved about 2 months after the acute illness. In a second case report, a previously healthy 39-year-old woman with a culture-confirmed C. jejuni infection developed redness and pain in her eyes about 4 weeks after the gastritis resolved (Howard et al. 1987). The eye condition was diagnosed as nonspecific anterior uveitis. The eye inflammation was treated and resolved over a period of 2 weeks. An HLA-B27 antigen test was negative. In the third case report, acute anterior uveitis was reported in a 34-year-old woman who had a culture-confirmed C. jejuni infection (Lever et al. 1984). She also had hypogammaglobulinemia and chronic diarrhea. No information was given on how the uveitis was treated, how long after onset of the infection the uveitis developed, or how long it took the condition to resolve. The committee concludes that there is limited or suggestive evidence of an association between C. jejuni infection and uveitis, if the uveitis is manifested within a month of the infection.

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Gulf War and Health: Volume 5. Infectious Diseases Nontyphoidal Salmonella Infection The genus Salmonella comprises commensal and pathogenic bacteria found in humans, mammals, reptiles, birds, and insects worldwide. These gram-negative, largely motile bacilli are highly adaptable facultative anaerobes 2-3 µm long that reside mainly in the intestines of their hosts. Salmonellae are classified in two species, S. enterica and S. bongori; the former is divided into six subspecies and more than 2,500 serotypes (or serovars) according to their somatic, surface, and flagellar antigens and their habitats (Box 5.1) (Center for Infectious Disease Research and Policy 2006; Pegues et al. 2005). BOX 5.1 Classification of Salmonella Salmonella enterica subspecies enterica (I) subspecies salmae (II) subspecies arizonae (IIIa) subspecies diarizonae (IIIb) subspecies houtenae (IV) subspecies indica (VI) Salmonella bongori SOURCE: Pegues et al. 2005. Salmonella enterica serotypes Typhi and Paratyphi cause life-threatening typhoid fever and paratyphoid fever (typhoidal salmonellosis), respectively. Those diseases’ severity, short incubation period, and other salient characteristics would lead to rapid detection, diagnosis, and treatment in deployed US military personnel (CDC 2005b; Olsen et al. 2003). In contrast, uncomplicated infection with nontyphoidal salmonellae causes an array of generally milder illnesses that appear similar to other diarrheal diseases and usually resolve without medical attention. Therefore, the committee devotes attention exclusively to infection with nontyphoidal salmonellae in this chapter. Transmission of Nontyphoidal Salmonellae Nontyphoidal salmonellae are most commonly transmitted by the ingestion of contaminated food, especially food of animal origin. Food derived from infected animals that is uncooked, inadequately cooked, unpasteurized, or inadequately pasteurized may transmit the bacteria to humans. Alternatively, such products may cross-contaminate other food that then becomes a vehicle for transmission. Outbreaks of salmonellosis also have arisen from the consumption of fresh produce contaminated with human or animal feces containing salmonellae (Pegues et al. 2005). Drinking contaminated water infrequently leads to transmission of nontyphoidal salmonellae to humans (Pegues et al. 2005). Exposure to salmonella-infected pets, especially reptiles, can lead to transmission to humans. Rarely, transmission occurs through the transfusion of tainted blood products (Wilson 1991).

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Gulf War and Health: Volume 5. Infectious Diseases Endemicity in Southwest and South-Central Asia Salmonella spp. is present in all countries (Wilson 1991). The centralized production and wide distribution of manufactured foods in developed nations periodically facilitates large outbreaks of salmonellosis (Pegues et al. 2005). Acute Illness Salmonella Gastroenteritis Gastroenteritis is the most common syndrome of infection with nontyphoidal Salmonella. Some 60-80% of cases occur sporadically. After an incubation period of 6-72 hours, patients experience sudden onset of diarrhea, nausea, and sometimes vomiting. Those symptoms are frequently accompanied by fever, headache, abdominal pain, and chills. Myalgia is sometimes reported. Rarely, patients manifest pseudoappendicitis or mimicry of the intestinal changes of inflammatory bowel disease (Heymann 2004; Pegues et al. 2005). Microscopic examination of stool specimens during the acute phase reveals neutrophils and sometimes red blood cells. Salmonella gastroenteritis is usually self-limited. Fever commonly resolves within 48-72 hours after onset. Diarrhea usually resolves within 3-7 days, after 10 days at most; however, patients continue to shed the agent in stool for 4-5 weeks, depending on the serotype of Salmonella. Patients who receive antimicrobial therapy may shed for longer periods (Pegues et al. 2005). Severe Salmonella gastroenteritis leads to dehydration and hospitalization in 2.2 cases per million in the US population. The disease causes about 580 deaths per year in the United States, primarily in elderly or immunocompromised people (Pegues et al. 2005). Salmonella Bacteremia Bacteremia occurs in 1-4% of immunocompetent patients who have Salmonella gastroenteritis. Any serotype of the agent may be responsible. Among adults, the risk of bacteremia is greater for Salmonella-infected people who are immunocompromised (Pegues et al. 2005). Diagnosis of Acute Illness Salmonella infection may be microbiologically confirmed by plating freshly passed stool samples onto a primary culture medium. Selenate-based enrichment broths can facilitate the recovery of low numbers of organisms. Rapid immunoglobulin M (IgM) antibody-based serologic tests may supplement stool culture (Pegues et al. 2005). Treatment of Acute Illness Uncomplicated gastroenteritis may be treated simply with ingestion of oral rehydration solution to replace water and electrolytes. Antibiotics are indicated in adults who are debilitated; who have HIV infection, continued fever, or high fever; or who manifest extraintestinal infection. Ciprofloxacin, ampicillin, or amoxicillin may be administered to adults. Trimethoprim-sulfamethoxazole and chloramphenicol may be effective for treating people who have microbial-resistant strains (Heymann 2004). Coinfection with Nontyphoidal Salmonellae and Human Immunodeficiency Virus Salmonellosis is sometimes the first manifestation of HIV infection. People with HIV are at much higher risk than the general population for salmonellosis, and the risk of Salmonella

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Gulf War and Health: Volume 5. Infectious Diseases bacteremia is 20-100 times greater. Salmonella bacteremia often recurs in HIV-infected people; indeed, such recurrence is a criterion for the classification of AIDS by the Centers for Disease Control and Prevention (CDC) (CDC 1992; Heymann 2004; Kim et al. 2004; Pegues et al. 2005). Long-Term Adverse Health Outcome of Nontyphoidal Salmonella Infection As discussed above, ReA is an acute nonpurulent form of arthritis that complicates infections at other sites of the body. The most commonly affected joints are the knees and ankles (Locht et al. 2002). If ReA follows an acute episode of nontyphoidal Salmonella infection, it is manifested 1-2 weeks after the gastrointestinal illness. The reported incidence of ReA among cases of acute nontyphoidal Salmonella infection ranges from only 1% to as high as 29% (Buxton et al. 2002; Dworkin et al. 2001; Hannu and Leirisalo-Repo 1988; Lee et al. 2005; Leirisalo-Repo et al. 1997; Locht et al. 1993; Locht et al. 2002; Maki-Ikola and Granfors 1992; Maki-Ikola et al. 1991; Maki-Ikola et al. 1992; Mattila et al. 1994; Mattila et al. 1998; Nikkari et al. 1999; Sinha et al. 2003; Thomas and Hedayati 1986; Thomson et al. 1994; Thomson et al. 1992; Thomson et al. 1995). Factors that influence the incidence include older age, longer duration of diarrhea, and the presence of HLA-B27. The duration of symptoms is variable, ranging from months to years (Lee et al. 2005; Leirisalo-Repo et al. 1997; Mattila et al. 1994; Thomson et al. 1995). Antibiotic treatment for the diarrheal illness does not affect the severity of ReA or its duration (Locht et al. 1993; Mattila et al. 1998). Ankylosing spondylitis occasionally follows ReA. ReA is a clinical diagnosis, but the presence of HLA-B27 is helpful. Symptom-based treatment involves primarily the administration of anti-inflammatory agents. The committee concludes that there is sufficient evidence of an association between nontyphoidal Salmonella infection and reactive arthritis (ReA) if the ReA is manifested within 3 months of the infection. Shigella Infection Like Campylobacter and nontyphoidal Salmonella infections, Shigella infections are common causes of acute diarrheal illnesses in humans globally (Halpern et al. 1989; Shears 1996; Taylor et al. 1991) and have been diagnosed in US troops during the Gulf War, OEF, and OIF. Occasionally, Shigella infections lead to long-term adverse health outcomes, notably ReA and hemolytic uremic syndrome. Each adverse health outcome appears to occur after an episode of shigellosis at frequencies greater than background rates. Transmission of Shigella Infection Humans are the reservoir for the four known species of Shigella: S. dysenteriae, S. flexneri, S. boydii, and S. sonnei. They are transmitted by the fecal-oral route and through fecal contamination of unpurified water, or uncooked or undercooked food. Person-to-person transmission is common and is facilitated by lack of hand-washing facilities and inadequate supply of potable water. In military camps, where sewerage is not regular, shigellosis may become epidemic. Although Shigella spp. occasionally infects other primates, such infections have little impact on transmission among humans.

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Gulf War and Health: Volume 5. Infectious Diseases Endemicity in Southwest and South-Central Asia Shigella is endemic, hyperendemic, or epidemic in locales with minimal sanitation. Shigellosis is well recognized in southwest and south-central Asia. S. flexneri and S. dysenteriae are more common in southwest and south-central Asia than in the United States, where S. sonnei dominates. Acute Illness Shigella infection causes an acute diarrheal illness. Symptoms are constitutional; they frequently include malaise and fever, and they immediately involve abdominal bloating, cramping, and diarrhea. During shigellosis, diarrhea may be nonbloody and watery or bloody; the latter condition is generally termed dysentery. Laboratory examination of stool specimens usually reveals numerous leukocytes. The number of loose stools can range from several per day to more than 20 on the worst day of the illness. Fever and constitutional symptoms typically peak during the period of most severe diarrheal symptoms. The diarrhea may be accompanied by tenesmus, or painful straining while defecating. The illness usually is self-limiting, and patients recover within a week. In the absence of antibiotic treatment, however, shigellosis can be severe or even, rarely, fatal (Bennish 1991). Diagnosis of Acute Illness Diagnosis is based on culture of fecal specimens and very rarely blood. When PCR methods are available, they can be equally valuable. People with acute shigellosis remain culture-positive for up to 4 weeks. Beyond that timeframe, culture is inadequate to confirm or refute any relationship of symptoms with Shigella. Treatment of Acute Illness Treatment of all acute gastrointestinal infections must be based first on fluid replacement. The use of antibiotics is recommended because it shortens the duration of shigellosis and the likelihood of transmission to other hosts (Bhattacharya and Sur 2003). Resistance to sulfonamides, chloramphenicol, and tetracyclines is nearly universal, and resistance to ampicillin and trimethoprim-sulfamethoxazole is frequent. Treatment with fluoroquinolines or azithromycin is successful, even in short courses (1-3 days). The use of antimotility agents may induce more severe disease and is contraindicated. Long-Term Adverse Health Outcomes of Shigella Infection Reactive Arthritis As discussed above, ReA is an acute nonpurulent form of arthritis that complicates infections at other sites of the body. If ReA follows an acute episode of shigellosis, it is usually manifested 2-3 weeks after the gastrointestinal illness (Calin and Fries 1976; Chen et al. 2002; Finch et al. 1986; Good 1979; Noer 1966; Sieper et al. 1993; Simon et al. 1981). It is most common after S. flexneri infection; it also follows infection by S. dysenteriae (Good 1979) but rarely S. sonnei (Good 1979; Kaslow RA 1979; Lewis 1982; Simon et al. 1981). Ankylosing spondylitis occasionally follows ReA and may be considered as a consequence of Shigella-induced ReA. The symptoms of ReA cause up to 25% of affected people to change or curtail their work. Followup studies suggest that some joint symptoms persist in 30-60% of patients for up to a year, but most patients recover within a few months (Calin and Fries 1976; Rongnoparat

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Gulf War and Health: Volume 5. Infectious Diseases Navarro-Martinez A, Solera J, Corredoira J, Beato JL, Martinez-Alfaro E, Atienzar M, Ariza J. 2001. Epididymoorchitis due to Brucella mellitensis: A retrospective study of 59 patients. Clinical Infectious Diseases 33(12):2017-2022. Navy Environmental Health Center. 2006. Preventive Medicine - Tuberculosis. [Online]. Available: http://www-nehc.med.navy.mil/prevmed/PM/PM_Tuberculosis.htm [accessed May 8, 2006]. Neithercut WD, Hudson MA, Smith CC. 1984. Can erythema nodosum and reactive arthritis be a sequel to Shigella flexneri gastroenteritis? Scottish Medical Journal 29(3):197-199. Nene A, Bhojraj S. 2005. Results of nonsurgical treatment of thoracic spinal tuberculosis in adults. The Spine Journal 5(1):79-84. Newman RD, Parise ME, Barber AM, Steketee RW. 2004. Malaria-related deaths among US travelers, 1963-2001. Annals of Internal Medicine 141(7):547-555. Niemeyer G, Fruh B. 1989. Examination strategies in the diagnosis of drug-induced retinal damage. Klinische Monatsblatter Fur Augenheilkunde 194(5):355-358. NIH (National Institutes of Health). 2002. Questions and Answers About Reactive Arthritis. National Institute of Arthritis and Musckuloskeletal Diseases (NIAMS), Public Health Service, US Department of Health and Human Services. Nikkari S, Rantakokko K, Ekman P, Mottonen T, Leirisalo-Repo M, Virtala M, Lehtonen L, Jalava J, Kotilainen P, Granfors K, Toivanen P. 1999. Salmonella-triggered reactive arthritis: Use of polymerase chain reaction, immunocytochemical staining, and gas chromatographymass spectrometry in the detection of bacterial components from synovial fluid. Arthritis and Rheumatism 42(1):84-89. Noer HR. 1966. An “experimental” epidemic of Reiter’s syndrome. Journal of the American Medical Association 198(7):693-698. Norton WL. 1984. Brucellosis and rheumatic syndromes in Saudi Arabia. Annals of the Rheumatic Diseases 43(6):810-815. Nourse C, Allworth A, Jones A, Horvath R, McCormack J, Bartlett J, Hayes D, Robson JM. 2004. Three cases of Q fever osteomyelitis in children and a review of the literature. Clinical Infectious Diseases 39(7):e61-e66. Oh MD, Shin H, Shin D, Kim U, Lee S, Kim N, Choi MH, Chai JY, Choe K. 2001. Clinical features of vivax malaria. American Journal of Tropical Medicine and Hygiene 65(2):143-146. Ohl CA, Hyams KC, Malone JD, Oldfield EC 3rd. 1993. Leishmaniasis among Desert Storm veterans: A diagnostic and therapeutic dilemma. Military Medicine 158(11):726-729. Okhuysen PC, Jiang ZD, Carlin L, Forbes C, DuPont HL. 2004. Post-diarrhea chronic intestinal symptoms and irritable bowel syndrome in North American travelers to Mexico. American Journal of Gastroenterology 99(9):1774-1778. Oldfield EC 3rd, Wallace MR, Hyams KC, Yousif AA, Lewis DE, Bourgeois AL. 1991. Endemic infectious diseases of the Middle East. Reviews of Infectious Diseases 13(3 Suppl):S199-S217. Oliveri R, Matera G, Foca A, Zappia M, Aguglia U, Quattrone A. 1996. Polyradiculoneuropathy with cerebrospinal fluid albuminocytological dissociation due to neurobrucellosis. Clinical Infectious Diseases 23(4):833-834.

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Gulf War and Health: Volume 5. Infectious Diseases Olsen SJ, Bleasdale SC, Magnano AR, Landrigan C, Holland BH, Tauxe RV, Mintz ED, Luby S. 2003. Outbreaks of typhoid fever in the United States, 1960-99. Epidemiology and Infection 130(1):13-21. Oren I, Kraoz Z, Hadani Y, Kassis I, Zaltzman-Bershadsky N, Finkelstein R. 2005. An outbreak of Q fever in an urban area in Israel. European Journal of Clinical Microbiology and Infectious Diseases 24(5):338-341. Papatsoris AG, Mpadra FA, Karamouzis MV, Frangides CY. 2002. Endemic brucellar epididymo-orchitis: A 10-year experience. International Journal of Infectious Diseases 6(4):309-313. Pappas G, Bosilkovski M, Akritidis N, Mastora M, Krteva L, Tsianos E. 2003. Brucellosis and the respiratory system. Clinical Infectious Diseases 37(7):e95-e99. Pappas G, Kitsanou M, Christou L, Tsianos E. 2004. Immune thrombocytopenia attributed to brucellosis and other mechanisms of Brucella-induced thrombocytopenia. American Journal of Hematology 75(3):139-141. Pappas G, Akritidis N, Bosilkovski M, Tsianos E. 2005. Brucellosis. New England Journal of Medicine 352(22):2325-2336. Parker NR, Barralet JH, Bell AM. 2006. Q fever. Lancet 367(9511):679-688. Parsonnet J, Griffin PM. 1993. Hemolytic uremic syndrome: Clinical picture and bacterial connection. Current Clinical Topics in Infectious Diseases 13:172-187. Parsonnet J, Greene KD, Gerber AR, Tauxe RV, Vallejo Aguilar OJ, Blake PA. 1989. Shigella dysenteriae type 1 infections in US travellers to Mexico, 1988. Lancet 2(8662):543-545. Pascual J, Combarros O, Polo JM, Berciano J. 1988. Localized CNS brucellosis: Report of 7 cases. Acta Neurologica Scandinavica 78(4):282-289. Pegues DA, Ohl ME, Miler SI. 2005. Salmonella species, including Salmonella typhi. In: Mandell GL, Bennett JE, Dolin R, Editors. Principles and Practice of Infectious Diseases. 6th ed. Philadelphia, PA: Elsevier. Pp. 2636-2654. Petersen LR, Roehrig JT. 2001. West Nile virus: A reemerging global pathogen. Emerging Infectious Diseases 7(4):611-614. Platonov AE. 2001. West Nile encephalitis in Russia 1999-2001: Were we ready? Are we ready? Annals of the New York Academy of Sciences 951:102-116. Plit ML, Anderson R, Van Rensburg CE, Page-Shipp L, Blott JA, Fresen JL, Feldman C. 1998. Influence of antimicrobial chemotherapy on spirometric parameters and pro-inflammatory indices in severe pulmonary tuberculosis. European Respiratory Journal 12(2):351-356. Portnoy JZ, Callen JP. 1983. Ophthalmologic aspects of chloroquine and hydroxychloroquine therapy. International Journal of Dermatology 22(5):273-278. Queipo-Ortuno MI, Morata P, Ocon P, Manchado P, Colmenero JD. 1997. Rapid diagnosis of human brucellosis by peripheral-blood PCR assay. Journal of Clinical Microbiology 35 (11):2927-2930. Rabinowitz R, Schneck M, Levy J, Lifshitz T. 2005. Bilateral multifocal choroiditis with serous retinal detachment in a patient with Brucella infection: Case report and review of the literature. Archives of Ophthalmology 123(1):116-118.

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Gulf War and Health: Volume 5. Infectious Diseases Rahaman MM, JamiulAlam AK, Islam MR, Greenough WB 3rd. 1975. Shiga bacillus dysentery associated with marked leukocytosis and erythrocyte fragmentation. Johns Hopkins Medical Journal 136(2):65-70. Raoult D. 2003. Use of macrolides for Q fever. Antimicrobial Agents and Chemotherapy 47(1):446. Raoult D, Piquet P, Gallais H, de Micco C, Drancourt M, Casanova P. 1986. Coxiella burnetii infection of a vascular prosthesis. New England Journal of Medicine 315(21):1358-1359. Raoult D, Levy PY, Dupont HT, Chicheportiche C, Tamalet C, Gastaut JA, Salducci J. 1993. Q fever and HIV infection. AIDS 7(1):81-86. Raoult D, Houpikian P, Tissot-Dupont H, Riss JM, Arditi-Djiane J, Brouqui P. 1999. Treatment of Q fever endocarditis: Comparison of 2 regimens containing doxycycline and ofloxacin or hydroxychloroquine. Archives of Internal Medicine 159(2):167-173. Raoult D, Tissot-Dupont H, Foucault C, Gouvernet J, Fournier PE, Bernit E, Stein A, Nesri M, Harle JR, Weiller PJ. 2000. Q fever 1985-1998. Clinical and epidemiologic features of 1,383 infections. Medicine 79(2):109-123. Raoult D, Fenollar F, Stein A. 2002. Q fever during pregnancy: Diagnosis, treatment, and follow-up. Archives of Internal Medicine 162(6):701-704. Raoult D, Marrie T, Mege J. 2005. Natural history and pathophysiology of Q fever. The Lancet Infectious Diseases 5(4):219-226. RBM (Roll Back Malaria). 2005a. Roll Back Malaria - Epidemiology. [Online]. Available: http://www.emro.who.int/rbm/Epidemiology-current.htm [accessed May 4, 2006]. RBM. 2005b. Roll Back Malaria - Regional Office for the Eastern Mediterranean: Epidemiological Situation. [Online]. Available: http://www.emro.who.int/rbm/epidemiology-2004.htm [accessed July 17, 2006]. RBM. 2005c. Roll Back Malaria - World Malaria Report: Afghanistan Country Profile. [Online]. Available: http://www.rbm.who.int/wmr2005/profiles/afghanistan.pdf [accessed May 4, 2006]. RBM. 2005d. Roll Back Malaria - World Malaria Report: Iran Country Profile. [Online]. Available at: http://www.rbm.who.int/wmr2005/profiles/iran.pdf [accessed May 5, 2006]. RBM. 2005e. Roll Back Malaria - World Malaria Report: Iraq Country Profile. [Online]. Available: http://www.rbm.who.int/wmr2005/profiles/iraq.pdf [accessed May 4, 2006]. RBM. 2005f. Roll Back Malaria - World Malaria Report: Pakistan Country Profile. [Online]. Available: http://www.rbm.who.int/wmr2005/profiles/pakistan.pdf [accessed May 4, 2006]. RBM. 2005g. Roll Back Malaria - World Malaria Report: Saudi Arabia Country Profile. [Online]. Available: http://www.rbm.who.int/wmr2005/profiles/saudiarabia.pdf [accessed May 4, 2006]. RBM. 2005h. Roll Back Malaria - World Malaria Report 2005 - Malaria Control, By Region. [Online]. Available: http://rbm.who.int/wmr2005/html/2-2.htm [accessed June 27, 2006]. Rees JH, Soudain SE, Gregson NA, Hughes RA. 1995. Campylobacter jejuni infection and Guillain-Barre syndrome. New England Journal of Medicine 333(21):1374-1379. Rees JR, Pannier MA, McNees A, Shallow S, Angulo FJ, Vugia DJ. 2004. Persistent diarrhea, arthritis, and other complications of enteric infections: A pilot survey based on California FoodNet surveillance, 1998-1999. Clinical Infectious Diseases 38(3 Suppl):S311-S17.

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Gulf War and Health: Volume 5. Infectious Diseases Renia L, Potter SM, Mauduit M, Rosa DS, Kayibanda M, Deschemin JC, Snounou G, Gruner AC. 2006. Pathogenic T cells in cerebral malaria. International Journal for Parasitology 36(5):547-554. Rhodes KM, Tattersfield AE. 1982. Guillain-Barre syndrome associated with Campylobacter infection. British Medical Journal (Clinical Research Ed.) 285(6336):173-174. Riestra-Castaneda R, Gonzalez-Garrido A, Gonzalez-Cornejo S. 1996. Brucellosis and polyneuroradiculomyeloencephalitis. A case report. Archives of Medical Research 27(3):331-333. Roehrig JT, Nash D, Maldin B, Labowitz A, Martin DA, Lanciotti RS, Campbell GL. 2003. Persistence of virus-reactive serum immunoglobulin m antibody in confirmed west nile virus encephalitis cases. Emerging Infectious Diseases 9(3):376-379. Roiz MP, Peralta FG, Valle R, Arjona R. 1998. Microbiological diagnosis of brucellosis. Journal of Clinical Microbiology 36(6):1819. Rolando I, Carbone A, Gotuzzo E, Carillo CP. 1985a. Circulating immune complexes in the pathogenesis of human brucellar uveitis. Chibret International Journal of Ophthalmology 3:30-38. Rolando I, Carbone A, Haro D, Gotuzzo E, Carrillo C. 1985b. Retinal detachment in chronic brucellosis. American Journal of Ophthalmology 99(6):733-734. Rolando I, Tobaru L, Hinostruza S. 1987. Clinical manifestations of 25 Brucella uveitis. Ophthalmic Practice 5:12-17. Rongnoparat C, Panpanit R. 1987. Hemolytic uremic syndrome associated with shigellosis: Report of two cases. Southeast Asian Journal of Tropical Medicine and Public Health 18(2):226-228. Ropper AH. 1988. Campylobacter diarrhea and Guillain-Barre syndrome. Archives of Neurology 45(6):655-656. Ruben B, Band JD, Wong P, Colville J. 1991. Person-to-person transmission of Brucella melitensis. Lancet 337(8732):14-15. Rubin M. 1968. Prolonged pharmacotherapy and the eye. A symposium. The antimalarials and the tranquilizers. Diseases of the Nervous System 29(3):S67-S76. Ruiz RS, Saatci OA. 1991. Chloroquine and hydroxychloroquine retinopathy: How to follow affected patients. Annals of Ophthalmology 23(8):290-291. Russo R, Laguna F, Lopez-Velez R, Medrano FJ, Rosenthal E, Cacopardo B, Nigro L. 2003. Visceral leishmaniasis in those infected with HIV: Clinical aspects and other opportunistic infections. Annals of Tropical Medicine and Parasitology 97(1 Suppl):99-105. Rynes RI, Bernstein HN. 1993. Ophthalmologic safety profile of antimalarial drugs. Lupus 2 (1 Suppl):S17-S19. Saad M, Youssef S, Kirschke D, Shubair M, Haddadin D, Myers J, Moorman J. 2005. Acute flaccid paralysis: The spectrum of a newly recognized complication of West Nile virus infection. Journal of Infection 51(2):120-127. Saah AJ. 2000. Introduction to rickettsioses and ehrlichioses. In: Mandell GL, Bennett JE, Dolin R, Editors. Principles and Practice of Infectious Diseases. 5th ed. New York: Churchill Livingstone. Pp. 2033-2035.

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Gulf War and Health: Volume 5. Infectious Diseases Sacks N, Van Rensburg AJ. 1976. Clinical aspects of chronic brucellosis. South African Medical Journal 50(19):725-728. Sanchez-Sousa A, Torres C, Campello MG, Garcia C, Parras F, Cercenado E, Baquero F. 1990. Serological diagnosis of neurobrucellosis. Journal of Clinical Pathology 43(1):79-81. Schlagenhauf P, Tschopp A, Johnson R, Nothdurft HD, Beck B, Schwartz E, Herold M, Krebs B, Veit O, Allwinn R, Steffen R. 2003. Tolerability of malaria chemoprophylaxis in non-immune travellers to sub-Saharan Africa: Multicentre, randomised, double blind, four arm study. British Medical Journal (Clinical Research Ed.) 327(7423):1078. Scrimgeour EM, Al-Ismaily SI, Rolain JM, Al-Dhahry SH, El-Khatim HS, Raoult D. 2003. Q Fever in human and livestock populations in Oman. Annals of the New York Academy of Sciences 990:221-225. Secretary of the Air Force. 2005. Air Force Instruction 48-105: Surveillance, Prevention, and Control of Diseases and Conditions of Public Health or Military Significance. Sejvar JJ, Haddad MB, Tierney BC, Campbell GL, Marfin AA, Van Gerpen JA, Fleischauer A, Leis AA, Stokic DS, Petersen LR. 2003. Neurologic manifestations and outcome of West Nile virus infection. Journal of the American Medical Association 290(4):511-515. Senanayake N, de Silva HJ. 1994. Delayed cerebellar ataxia complicating falciparum malaria: A clinical study of 74 patients. Journal of Neurology 241(7):456-459. Shamo FJ. 2001. Malaria in Iraq. Meditsinskaia Parazitologiia i Parazitarnye Bolezni (1):46-47. Shanks GD, Edstein MD. 2005. Modern malaria chemoprophylaxis. Drugs 65(15):2091-2110. Shears P. 1996. Shigella infections. Annals of Tropical Medicine and Parasitology 90(2):105-114. Shibukawa-Kent R. 2006. Air Force Institute for Operational Health. Personal communication. Shubhakaran, Sharma CM. 2003. Acute inflammatory demyelinating polyneuropathy with P. falciparum malaria. Journal of the Association of Physicians of India 51:223-224. Shute PG, Lupascu G, Branzei P, Maryon M, Constantinescu P, Bruce-Chwatt LJ, Draper CC, Killick-Kendrick R, Garnham PC. 1977. A strain of Plasmodium vivax characterized by prolonged incubation: The effect of numbers of sporozoites on the length of the prepatent period. Transactions of the Royal Society of Tropical Medicine and Hygiene 70(5-6):474-481. Siegman-Igra Y, Kaufman O, Keysary A, Rzotkiewicz S, Shalit I. 1997. Q fever endocarditis in Israel and a worldwide review. Scandinavian Journal of Infectious Diseases 29(1):41-49. Sieper J, Braun J, Wu P, Hauer R, Laitko S. 1993. The possible role of Shigella in sporadic enteric reactive arthritis. British Journal of Rheumatology 32(7):582-585. Simon DG, Kaslow RA, Rosenbaum J, Kaye RL, Calin A. 1981. Reiter’s syndrome following epidemic shigellosis. Journal of Rheumatology 8(6):969-973. Sinha R, Aggarwal A, Prasad K, Misra R. 2003. Sporadic enteric reactive arthritis and undifferentiated spondyloarthropathy: Evidence for involvement of Salmonella typhimurium. Journal of Rheumatology 30(1):105-113. Sinha S, Prasad KN, Pradhan S, Jain D, Jha S. 2004. Detection of preceding Campylobacter jejuni infection by polymerase chain reaction in patients with Guillain-Barre syndrome. Transactions of the Royal Society of Tropical Medicine and Hygiene 98(6):342-346.

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Gulf War and Health: Volume 5. Infectious Diseases Skirrow MB, Blaser MJ. 2002. Campylobacter jejuni. In: Blaser MJ, Smith PD, Raudin JI, Greenberg HB, Guerrant RL, Editors. Infections of the Gastrointestinal Tract. 2nd ed. Philadelphia, PA: Lippincott. Pp. 719-739. Smith B, Ryan MA, Gray GC, Polonsky JM, Trump DH. 2002. Tuberculosis infection among young adults enlisting in the United States Navy. International Journal of Epidemiology 31(5):934-939. Smith DL, Ayres JG, Blair I, Burge PS, Carpenter MJ, Caul EO, Coupland B, Desselberger U, Evans M, Farrell ID, et al. 1993. A large Q fever outbreak in the West Midlands: Clinical aspects. Respiratory Medicine 87(7):509-516. Solera J, Rodriguez-Zapata M, Geijo P, Largo J, Paulino J, Saez L, Martinez-Alfaro E, Sanchez L, Sepulveda MA, Ruiz-Ribo MD. 1995. Doxycycline-rifampin versus doxycycline-streptomycin in treatment of human brucellosis due to Brucella melitensis. The GECMEI Group. Grupo de Estudio de Castilla-la Mancha de Enfermedades Infecciosas. Antimicrobial Agents and Chemotherapy 39(9):2061-2067. Solera J, Lozano E, Martinez-Alfaro E, Espinosa A, Castillejos ML, Abad L. 1999. Brucellar spondylitis: Review of 35 cases and literature survey. Clinical Infectious Diseases 29(6):1440-1449. Solomon T, Cardosa MJ. 2000. Emerging arboviral encephalitis. Newsworthy in the West but much more common in the East. British Medical Journal (Clinical Research Ed.) 321(7275):1484-1485. Speed B, Kaldor J, Cavanagh P. 1984. Guillain-Barre syndrome associated with Campylobacter jejuni enteritis. Journal of Infection 8(1):85-86. Spink WW. 1951. What is chronic brucellosis? Annals of Internal Medicine 35(2):358-374. Spink WW. 1954. Family studies on brucellosis. American Journal of the Medical Sciences 227(2):128-133. Stead WW, Dutt AK. 1991. Tuberculosis in elderly persons. Annual Review of Medicine 42: 267-276. Stead WW, Lofgren JP. 1983. Does the risk of tuberculosis increase in old age? Journal of Infectious Diseases 147(5):951-955. Stead WW, To T. 1987. The significance of the tuberculin skin test in elderly persons. Annals of Internal Medicine 107(6):837-842. Stein A, Raoult D. 1995. Q fever endocarditis. European Heart Journal 16(B Suppl):19-23. Sugamata M, Ahmed A, Miura T, Takasu T, Kono R, Ogata T, Kimura-Kuroda J, Yasui K. 1988. Seroepidemiological study of infection with West Nile virus in Karachi, Pakistan, in 1983 and 1985. Journal of Medical Virology 26(3):243-247. Sugiyama T, Okazaki T, Yabe Y, Suda H, Saito T. 1967. Basic and clinical study on chloroquine therapy of rheumatic diseases. Eye disorders due to chloroquine. Saishin Igaku. Recent Medicine 22(10):2331-2335. Sundar S, Agrawal S, Pai K, Chance M, Hommel M. 2005. Detection of leishmanial antigen in the urine of patients with visceral leishmaniasis by a latex agglutination test. American Journal of Tropical Medicine and Hygiene 73(2):269-271. Sutlas PN, Unal A, Forta H, Senol S, Kirbas D. 2003. Tuberculous meningitis in adults: Review of 61 cases. Infection 31(6):387-391.

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Gulf War and Health: Volume 5. Infectious Diseases Svedhem A, Kaijser B. 1980. Campylobacter fetus subspecies jejuni: A common cause of diarrhea in Sweden. Journal of Infectious Diseases 142(3):353-359. Tabbara KF. 1990. Brucellosis and nonsyphilitic treponemal uveitis. International Ophthalmology Clinics 30(4):294-296. Tam CC, Rodrigues LC, O'Brien SJ. 2003. Guillain-Barre syndrome associated with Campylobacter jejuni infection in England, 2000-2001. Clinical Infectious Diseases 37(2):307-310. Tardei G, Ruta S, Chitu V, Rossi C, Tsai TF, Cernescu C. 2000. Evaluation of immunoglobulin M (IgM) and IgG enzyme immunoassays in serologic diagnosis of West Nile Virus infection. Journal of Clinical Microbiology 38(6):2232-2239. Tasova Y, Saltoglu N, Sahin G, Aksu HS. 1999. Osteoarthricular involvement of brucellosis in Turkey. Clinical Rheumatology 18(3):214-219. Tauxe RV, Blake PA. 1992. Epidemic cholera in Latin America. Journal of the American Medical Association 267(10):1388-1390. Taylor JP, Perdue JN. 1989. The changing epidemiology of human brucellosis in Texas, 1977-1986. American Journal of Epidemiology 130(1):160-165. Taylor WR, White NJ. 2004. Antimalarial drug toxicity: A review. Drug Safety 27(1):25-61. Taylor DN, Echeverria P, Pitarangsi C, Seriwatana J, Bodhidatta L, Blaser MJ. 1988. Influence of strain characteristics and immunity on the epidemiology of Campylobacter infections in Thailand. Journal of Clinical Microbiology 26(5):863-868. Taylor DN, Bodhidatta L, Echeverria P. 1991. Epidemiologic aspects of shigellosis and other causes of dysentery in Thailand. Reviews of Infectious Diseases 13(4):S226-S230. Teixeira MJ, Teixeira CR, Andrade BB, Barral-Netto M, Barral A. 2006. Chemokines in host-parasite interactions in leishmaniasis. Trends in Parasitology 22(1):32-40. Thomas MF, Hedayati H. 1986. Reactive arthropathy (Reiter's syndrome) after salmonellosis: Report of two cases and review of the literature. Journal of the American Osteopathic Association 86(8):504-507. Thomas R, Kameswaran M, Murugan V, Okafor BC. 1993. Sensorineural hearing loss in neurobrucellosis. Journal of Laryngology and Otology 107(11):1034-1036. Thomson GT, Chiu B, De Rubeis D, Falk J, Inman RD. 1992. Immunoepidemiology of post-Salmonella reactive arthritis in a cohort of women. Clinical Immunology and Immunopathology 64(3):227-232. Thomson GT, Alfa M, Orr K, Thomson BR, Olson N. 1994. Secretory immune response and clinical sequelae of Salmonella infection in a point source cohort. Journal of Rheumatology 21(1):132-137. Thomson GT, DeRubeis DA, Hodge MA, Rajanayagam C, Inman RD. 1995. Post-Salmonella reactive arthritis: Late clinical sequelae in a point source cohort. American Journal of Medicine 98(1):13-21.

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Gulf War and Health: Volume 5. Infectious Diseases Thwaites GE, Duc Bang N, Huy Dung N, Thi Quy H, Thi Tuong Oanh D, Thi Cam Thoa N, Quang Hien N, Tri Thuc N, Ngoc Hai N, Thi Ngoc Lan N, Ngoc Lan N, Hong Duc N, Ngoc Tuan V, Huu Hiep C, Thi Hong Chau T, Phuong Mai P, Thi Dung N, Stepniewska K, Simmons CP, White NJ, Tinh Hien T, Farrar JJ. 2005. The influence of HIV infection on clinical presentation, response to treatment, and outcome in adults with Tuberculous meningitis. Journal of Infectious Diseases 192(12):2134-2141. Tissot-Dupont H, Raoult D, Brouqui P, Janbon F, Peyramond D, Weiller PJ, Chicheportiche C, Nezri M, Poirier R. 1992. Epidemiologic features and clinical presentation of acute Q fever in hospitalized patients: 323 French cases. American Journal of Medicine 93(4):427-434. Tissot-Dupont H, Amadei MA, Nezri M, Raoult D. 2004. Wind in November, Q fever in December. Emerging Infectious Diseases 10(7):1264-1269. Toler SM. 2004. Oxidative stress plays an important role in the pathogenesis of drug-induced retinopathy. Experimental Biology and Medicine (Maywood, NJ) 229(7):607-615. Travis LB, Travis WD, Li CY, Pierre RV. 1986. Q fever. A clinicopathologic study of five cases. Archives of Pathology and Laboratory Medicine 110(11):1017-1020. Tripathi BM, Dube S, Biseria S. 1995. Ophthalmic involvement in severe malaria. Journal of the Association of Physicians of India 43(6):441-442. Trujillo IZ, Zavala AN, Caceres JG, Miranda CQ. 1994. Brucellosis. Infectious Disease Clinics of North America 8(1):225-241. Turck WP, Howitt G, Turnberg LA, Fox H, Longson M, Matthews MB, Das Gupta R. 1976. Chronic Q fever. Quarterly Journal of Medicine 45(178):193-217. Turgut M. 2001. Spinal tuberculosis (Pott's disease): Its clinical presentation, surgical management, and outcome. A survey study on 694 patients. Neurosurgical Review 24(1): 8-13. Tzekov R. 2005. Ocular toxicity due to chloroquine and hydroxychloroquine: Electrophysiological and visual function correlates. Documenta Ophthalmologica 110(1):111-120. Vallejo JG, Stevens AM, Dutton RV, Kaplan SL. 1996. Hepatosplenic abscesses due to Brucella melitensis: Report of a case involving a child and review of the literature. Clinical Infectious Diseases 22(3):485-489. van Woerden HC, Mason BW, Nehaul LK, Smith R, Salmon RL, Healy B, Valappil M, Westmoreland D, de Martin S, Evans MR, Lloyd G, Hamilton-Kirkwood M, Williams NS. 2004. Q fever outbreak in industrial setting. Emerging Infectious Diseases 10(7):1282-9. Varney NR, Roberts RJ, Springer JA, Connell SK, Wood PS. 1997. Neuropsychiatric sequelae of cerebral malaria in Vietnam veterans. Journal of Nervous and Mental Disease 185(11):695-703. Verdon R, Chevret S, Laissy JP, Wolff M. 1996. Tuberculous meningitis in adults: Review of 48 cases. Clinical Infectious Diseases 22(6):982-988. Vynnycky E, Fine PE. 1997. The natural history of tuberculosis: The implications of age-dependent risks of disease and the role of reinfection. Epidemiology and Infection 119(2):183-201. Walker J, Sharma OP, Rao NA. 1992. Brucellosis and uveitis. American Journal of Ophthalmology 114(3):374-375.

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Gulf War and Health: Volume 5. Infectious Diseases Wallace MR, Hale BR, Utz GC, Olson PE, Earhart KC, Thornton SA, Hyams KC. 2002. Endemic infectious diseases of Afghanistan. Clinical Infectious Diseases 34(Suppl 5):S171-S207. Watson JT, Pertel PE, Jones RC, Siston AM, Paul WS, Austin CC, Gerber SI. 2004. Clinical characteristics and functional outcomes of West Nile Fever. Annals of Internal Medicine 141(5):360-365. Wei LC, Chen SN, Ho CL, Kuo YH, Ho JD. 2001. Progression of hydroxychloroquine retinopathy after discontinuation of therapy: Case report. Chang Gung Medical Journal 24(5):329-334. Weil Y, Mattan Y, Liebergall M, Rahav G. 2003. Brucella prosthetic joint infection: A report of 3 cases and a review of the literature. Clinical Infectious Diseases 36(7):e81-e86. Weina PJ, Neafie RC, Wortmann G, Polhemus M, Aronson NE. 2004. Old world leishmaniasis: An emerging infection among deployed US military and civilian workers. Clinical Infectious Diseases 39(11):1674-1680. WHO (World Health Organization). 1986. Joint FAO/WHO expert committee on brucellosis. World Health Organization Technical Report Series 740:1-132. WHO. 2002. Strategic Direction for Research: Leishmaniasis. Geneva: World Health Organization. WHO. 2003. Africa Malaria Report 2003. [Online]. Available: http://www.rbm.who.int/amd2003/amr2003/amr_toc.htm [accessed May 2, 2005]. WHO. 2004. Anti-Tuberculosis Drug Resistance in the World Report No. 3. Geneva: World Health Organization. WHO. 2006a. WHO Report 2006: Global Tuberculosis Control Surveillance, Planning, Financing. Geneva: World Health Organization. WHO. 2006b. Tuberculosis Fact Sheet No 104. [Online]. Available: http://www.who.int/mediacentre/factsheets/fs104/en/print.html [accessed May 1, 2006]. Wildman MJ, Smith EG, Groves J, Beattie JM, Caul EO, Ayres JG. 2002. Chronic fatigue following infection by Coxiella burnetii (Q fever): Ten-year follow-up of the 1989 UK outbreak cohort. QJM 95(8):527-538. Willard RJ, Jeffcoat AM, Benson PM, Walsh DS. 2005. Cutaneous leishmaniasis in soldiers from Fort Campbell, Kentucky returning from Operation Iraqi Freedom highlights diagnostic and therapeutic options. Journal of the American Academy of Dermatology 52(6):977-987. Williams RK, Crossley K. 1982. Acute and chronic hepatic involvement of brucellosis. Gastroenterology 83(2):455-458. Wilson ME. 1991. A World Guide to Infections: Diseases, Distribution, Diagnosis. New York: Oxford University Press. Wilson PE, Alker AP, Meshnick SR. 2005. Real-time PCR methods for monitoring antimalarial drug resistance. Trends in Parasitology 21(6):278-283. Wortmann G. 2004. Pulmonary manifestations of other agents: Brucella, Q fever, tularemia and smallpox. Respiratory Care Clinics of North America 10(1):99-109. Yebra M, Marazuela M, Albarran F, Moreno A. 1988. Chronic Q fever hepatitis. Reviews of Infectious Diseases 10(6):1229-1230.

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Gulf War and Health: Volume 5. Infectious Diseases Yechoor VK, Shandera WX, Rodriguez P, Cate TR. 1996. Tuberculous meningitis among adults with and without HIV infection. Experience in an urban public hospital. Archives of Internal Medicine 156(15):1710-1716. Young EJ. 1983. Human brucellosis. Reviews of Infectious Diseases 5(5):821-842. Young EJ. 1991. Serologic diagnosis of human brucellosis: Analysis of 214 cases by agglutination tests and review of the literature. Reviews of Infectious Diseases 13(3):359-372. Young EJ, Tarry A, Genta RM, Ayden N, Gotuzzo E. 2000. Thrombocytopenic purpura associated with brucellosis: Report of 2 cases and literature review. Clinical Infectious Diseases 31(4):904-909. Yu D, Kuipers JG. 2003. Role of bacteria and HLA-B27 in the pathogenesis of reactive arthritis. Rheumatic Diseases Clinics of North America 29(1):21-36, v-vi. Zaks N, Sukenik S, Alkan M, Flusser D, Neumann L, Buskila D. 1995. Musculoskeletal manifestations of brucellosis: A study of 90 cases in Israel. Seminars in Arthritis and Rheumatism 25(2):97-102. Zijlstra EE, Musa AM, Khalil EA, el-Hassan IM, el-Hassan AM. 2003. Post-kala-azar dermal leishmaniasis. The Lancet Infectious Dieases 3(2):87-98. Zinneman HH, Glenchur H, Hall WH. 1961. Chronic renal brucellosis. New England Journal of Medicine 265:872-875.

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