Physicians treating patients who have returned from deployments to Iraq, Afghanistan and Kuwait should be aware of some unique, possible exposures of this population. For example, service members could return home with diseases that are rarely seen in the United States, including infectious diseases that may not be apparent for some time after they first return.

While documenting medical history, it is critical that veterans be queried about where they have been, any symptoms or acute diseases they experienced during or after deployment, compliance with prophylactic medications and immunizations, any unusual environmental conditions they recall, and other items that you might normally consider when questioning about international travel and high-risk occupations.

Diseases that civilian physicians like you may encounter in this patient population can be considered in three broad categories:

• Common conditions that may or may not occur at a higher incidence in recently returned veterans, and for which the deployment may be either unrelated or an aggravating factor (e.g., chronic skin or respiratory problems
• Diseases rarely seen in U.S. clinics or hospitals, but which occur fairly frequently in those who have served in Southwest or Central Asia (e.g., cutaneous leishmaniasis)
• Diseases that are relatively uncommon even among veterans of Iraq and Afghanistan but which, if missed or not appropriately treated, could have serious consequences (e.g., visceral leishmaniasis, falciparum malaria, Q fever and acute eosinophilic pneumonia)

This overview is by no means comprehensive, but it is meant to highlight three conditions that most U.S. providers are unlikely to have experience diagnosing or managing. This is not intended to be a definitive guide for these conditions, so you should pursue other sources for more clinical information (e.g., specific diagnostic tests, drugs of choice and dosages, etc.), as you would for any disease you do not normally encounter. A bit more space is devoted here to acute eosinophilic pneumonia simply because there is less literature generally available on this syndrome.

Cutaneous leishmaniasis (CL), an infection by protozoan parasites of the genus Leishmania, is being seen in increasing numbers of military and civilian personnel who have been deployed to Iraq, Kuwait and Afghanistan.

The parasite is inoculated into the skin by the bite of an infected sand fly. The incubation period is usually two to eight weeks, but may be years, depending on initial inoculum size.

Symptoms and signs are an inflammatory papule or nodule that slowly increases in size and ulcerates. Lesions may be hyperkeratotic and do not always ulcerate. There may be involvement of proximal lymph nodes. Psoriasiform, vesicular and eczematous lesions are not likely to be cutaneous leishmaniasis. The base will crust over, but the ulcer spreads under the edge of a firm and raised border. Lesions are usually on exposed skin (where sand flies might bite) and are rarely seen in the scalp or on the palms and soles.

Laboratory confirmation requires demonstration of the parasite (or PCR in a specialized laboratory). To obtain a specimen, first clean the ulcer base, then scrape the base and place scrapings onto a glass slide, and stain with Giemsa or Diff-Quick. Prepare Giemsa stained touch preps using a small full thickness skin biopsy from the lesion’s edge. Divide the biopsy specimen longitudinally into halves for culture and histology. The diagnosis must be confirmed before treatment is offered.

Currently, antimony-based compounds are the drugs of choice for treatment of complicated CL. Treatment is generally with pentavalent antimonials, such as Pentostam® (sodium stibogluconate).

For detailed information on leishmaniasis diagnosis and treatment, refer to the following Web site information:

1. Army Policy for Management of Suspected Cutaneous Leishmaniasis , Office of The Surgeon General, 10 Sept 2004
   • Appendix 1, Clinical Policy Guidance for the Management of Suspected Cases of Cutaneous Leishmanasis in Operation Iraqi Freedom and Operation Enduring Freedom
   • Appendix 2, Leishmania Scraping and Biopsy Procedures
2. Updated information paper, Emerging Health Issues: Leishmaniasis among Soldiers in OIF/OEF, 10 March 2005.

Military and civilian health care providers may encounter malaria in service members and civilians returning from deployments in Afghanistan and Iraq. Malaria is transmitted by bites of infected anopheline mosquitoes and varies seasonally and geographically in these deployment areas. In the indigenous population in Afghanistan and Iraq, Plasmodium vivax accounts for 80 and 95 percent of diseases, respectively. Plasmodium falciparum is the cause of remaining cases. (These numbers may not be up-to-date due to relatively unreliable reporting in recent years because of conflicts and war in the countries.)

Malaria can present as soon as five days after arrival in an endemic area, and anytime thereafter, under conditions of continuous exposure. The usual incubation period for P. vivax is 14 days, but it can range from 12 days to 10 months even if a patient had been thoroughly compliant with prophylactic medication during deployment (to supress blood-stage malaria) and a two-week course of primaquine after departing the theater (to eradicate persistent hepatic parasites). Primaquine should be included in the treatment regimen for individuals with documented P. vivax malaria. Primaquine should not be given to pregnant or G6PD-deficient individuals. For more on treatment, see the CDC’s treatment guidelines.

Acute Eosinophilic Pneumonia (AEP)

Acute eosinophilic pneumonia (AEP) is one of a heterogeneous group of disorders collectively termed the eosinophilic pneumonias or eosinophilic lung diseases. These disorders are characterized by eosinophilic infiltration of the lung, which may or may not be accompanied by peripheral blood eosinophilia. Eosinophilic pneumonia may be seen in association with a diverse group of known clinical disorders, including parasitic and fungal infections, immunologic and systemic diseases, and drug toxicity. These secondary forms can present as simple, acute or chronic eosinophilic pneumonia. In the absence of an identifiable cause, simple, acute and chronic eosinophilic pneumonia may also be idiopathic.

Eosinophilic lung disease can be diagnosed by several means. Infiltrates on chest radiographs combined with peripheral blood eosinophilia can be used to define eosinophilic pneumonia; however, this indirect approach has two limitations. First, peripheral blood eosinophilia does not prove that infiltrates on chest radiographs are eosinophilic in origin, and second, eosinophilic infiltration of the lung is not always accompanied by peripheral blood eosinophilia. More directly, pulmonary eosinophilia can be assessed using bronchoalveolar lavage (BAL) or lung biopsy (open or transbronchial).

Patients with AEP typically present with an acute respiratory illness of one- to seven-days duration, manifested by fever, dyspnea, cough, pleuritic chest pain, myalgias, crackles on chest auscultation, hypoxemic respiratory insufficiency, bilateral diffuse infiltrates on chest radiographs, and increased eosinophils in BAL fluid or lung biopsy. Respiratory insufficiency progresses to respiratory failure requiring mechanical ventilation in a high percentage of cases.

AEP may be mistaken for other diseases, particularly community-acquired pneumonia, resulting in delayed or missed diagnosis. As defined by the North American-European Consensus Committee, many patients with AEP meet the criteria for acute lung injury ALI), including its most severe subset—acute respiratory distress syndrome (ARDS). Distinguishing AEP from other conditions underlying ARDS, and from infectious pneumonia, is critical because of differences in response to corticosteroids and outcome. Patients with AEP characteristically show a rapid response to corticosteroids and have an excellent prognosis resulting in a favorable outcome in most patients, whereas non-AEP patients with ARDS do not benefit from corticosteroid therapy and have a poor prognosis with mortality rates reported to range from 10 percent to 90 percent.  Peripheral blood eosinophil counts may be normal; however, 19 of 27 (70 percent) patients described in separate studies by Umeki and Philit had peripheral blood eosinophilia greater than 0.5 x 109 per Liter (500 per mm3) at some point during the course of illness. Thus, the presence or absence of peripheral blood eosinophilia is of questionable value in diagnosing AEP, but it may serve an important clue to guide additional, clinical steps particularly if the patient is already receiving antimicrobial therapy for a presumed infectious process, but not improving. BAL fluid provides an even more important clue to the diagnosis of AEP. BAL fluid eosinophilic percentages and total numbers are markedly increased in AEP, whereas ARDS is usually associated with increased neutrophils, and most viral and bacterial pneumonias typically are not characterized by BAL eosinophilia. In the appropriate clinical setting, BAL eosinophilia is itself adequate justification for a trial of corticosteroids without tissue biopsy. When BAL eosinophilia is present, the patient should be evaluated for known causes of pulmonary eosinophilia. BAL fluid should be cultured and stained for infectious agents, as the most important point in the differential diagnosis is the exclusion of an infectious process.

The radiologic findings in AEP are similar to those of pulmonary edema, but other considerations in the radiologic differential diagnosis include pulmonary hemorrhage and either viral or atypical bacterial pneumonia.

AEP is associated with a variety of clinical disorders, including fungal and parasitic infections, immunologic and systemic diseases and drug toxicity. AEP has been strongly associated with initiation of cigarette smoking (or re-initiation after prior cessation). It has also been associated with inhalation of various agents, including dust, Scotchguard, heroin and smoke from fireworks. Although many associations are known, the exact cause or causes and the mechanism by which eosinophils are recruited into the lungs in AEP are unclear.

At least 20 troops serving in Operation Iraqi Freedom or Operation Enduring Freedom have developed AEP. These were typically new-onset smokers, but without another, consistent exposure that set them apart from non-cases in a statistically significant manner. Still, ubiquitous conditions—such as high environmental particulate levels, or dusts or volatile organics associated with new construction—may have selectively induced AEP in genetically susceptible individuals whose lungs were “set up” by the immunological or physiological response to tobacco smoke. The deployment of such a large number of troops, combined with the significant increases in tobacco use that can be associated with deployments, may have further contributed to the clustering of otherwise rare cases.

AEP patients respond rapidly to corticosteroids and do not relapse once corticosteroids are discontinued. Spontaneous recovery also occurs.

References:

Weina PJ, Neafie RC, Wortmann G, Polhemus M, Aronson NE. Old world Leishmaniasis: an emerging infection among deployed US military and civilian workers. Clin Infect Dis 2004;39:1674-1680.

Leishmaniasis among U.S. Armed Forces, January 2003–November 2004. Medical Surveillance Monthly Report, Page 2. http://amsa.army.mil/1MSMR/2004/v10_no06.pdf.

Malaria, US Army, 2004, Medical Surveillance Monthly Report, Page 7.  http://amsa.army.mil/1MSMR/2005/v11_no01.pdf.

Kotwal RS, Wenzel RB, Sterling RA, Porter WD, Jordan NN, Petruccelli BP. An outbreak of malaria in US Army Rangers returning from Afghanistan. JAMA 2005;293:212-216.

Shorr AF, Scoville SL, Cersovsky SB, Shanks GD, Ockenhouse CF, Smoak BL, Carr WW, Petruccelli BP. Acute eosinophilic pneumonia among US military personnel deployed in or near Iraq. JAMA 2004;292:2997-3005.

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