In the series referred to above, there were 13 patients in the acute septicemic phase, seven of whom died shortly after admission. Nine patients were classified as subacute, all of whom subsequently recovered. Five patients were relatively asymptomatic (subclinical infection) and three initially had chronic or extrapulmonary manifestations of the disease with symptoms related to the involved area. All three recovered, although one had a complicated clinical course.

There is some difficulty in separating patients by symptoms alone (as in the acute and subacute categories), but the importance of doing so is readily apparent. The treatment, prognosis and subsequent mortality are often quite different in each category. Because the disease can fluctuate, it is necessary to recognize changes and institute more satisfactory treatment where necessary.

The acute or septicemic form of melioidosis is associated with a high mortality, even after intensive therapy. These patients are usually quite toxic with chills, high fever, severe headache and muscle tenderness, productive cough, hemoptysis, pleuritic pain, diarrhea and malaise. Progressive prostration, disorientation, dyspnea, pulmonary consolidation, and hepatosplenomegaly associated with septicemia usually lead to death in a few days, unless vigorous antibiotic therapy is promptly instituted. Delirium and mania are frequent terminal symptoms.

The lungs are the most common site of involvement in acute melioidosis, with necrotizing pneumonia and multiple small abscesses, but few organs remain uninfected. Septic emboli are frequently disseminated throughout the body. There may be signs of arthritis and meningitis. Gastrointestinal symptoms may suggest dysentery, cholera, or typhoid fever. Pulmonary manifestations may mimic tuberculosis, lobar or staphylococcal pneumonia, or lung abscess. Occasionally, a severe pyelonephritis or cystitis may occur or, rarely, be the presenting manifestation. Acute suppurative parotitis, often leading to parotid abscess, is a characteristic presentation of acute melioidosis in children, especially in northeast Thailand. Puthucheary et al found chronic underlying disease such as diabetes, renal disease, systemic lupus, malignancy and other diseases associated with a compromised immune system to be predisposing factors in 76% of 50 Malaysian patients with septicemic melioidosis.

The subacute form of this disease has milder symptoms and a longer prodromal period of weeks to months. Patients usually complain of cough, pleuritic chest pain, intermittent fever and weight loss. The initial lesion is often cutaneous or subcutaneous with subsequent hematological dissemination. These patients are more responsive to therapy than the acute group, but will occasionally progress to the acute stage if not adequately treated. Patients in this group may initially be diagnosed as having tuberculosis (Figs. 23.13-23.16). A serologic survey of 275 Chinese patients in a Hong Kong tuberculosis sanitorium revealed that 14% had hemagglutinin titers for melioidosis of 1:80 or higher.

Most patients with the subclinical form of melioidosis are asymptomatic. A few patients have symptoms probably unrelated to melioidosis; as part of their diagnostic evaluation, abnormalities may be detected on chest roentgenograms and melioidosis confirmed later by laboratory tests. The subclinical type is now thought to be the most common form of melioidosis, with an evolutional history similar to the eventual recognition of various chronic fungal infections. The initial diagnosis may be tuberculosis, but a history suggesting previous melioidosis or residence in the endemic area can be obtained from most of these patients. The subclinical form may remain dormant in individuals for many years and then may be reactivated, with possible dissemination when host resistance is compromised (Fig. 23.22). It is of interest to note that most of the occasional cases of melioidosis reported in countries other than Southeast Asia and Oceania are of the subclinical or chronic type in patients who once resided in or visited the endemic area months or years earlier.

The chronic, usually extrapulmonary presentation of melioidosis can be either bloodborne (from the lungs) or begin as a localized cutaneous lesion, with infection usually spreading via the lymphatics with lymph node involvement. Although the initial site of infection may be small, the surrounding erythema and host reaction may be quite large. Occasionally there may be subcutaneous and deep abscesses, draining sinuses, septic arthritis, or osteomyelitis (Figs. 23.23, 23.24). Coalescent nodules and purulent abscesses may be found in the liver (the disease can rarely present as a liver abscess and be mistaken for amebiasis), lungs, myocardium, spleen (Fig. 23.25), kidneys and brain (with meningitis). These cases can be relatively resistant to therapy and, with deep organ involvement, may occasionally terminate fatally. Fortunately the chronic or extrapulmonary form of melioidosis (excluding primary skin lesions) is relatively rare. When it does occur, it is usually a sequel to either a previously unrecognized or quiescent subacute infection or recrudescence of a prior symptomatic, probably inadequately treated, acute or subacute infection (in one patient, 26 years later). In this form of melioidosis, there still exists the potential for sudden exacerbation, with the disease reverting to the acute or subacute form. AIDS and other immunocompromised states have been reported as precursors to recrudescent melioidosis in Thailand.