Bacterial Diseases Lar Walls
The gross lesions resemble the bronchopneumonia of tuberculosis,' although histologically there is less epithelioid cell transformation. Tubercle-like nodules are more common in lymph nodes than in the lungs. Mediastinal nodes are involved frequently. Bacterial Diseases Clinical manifestations. The pertinent his-toric and epidemiologic features are often helpful clues, and in approximately three-fourths of all patients, there is a primary lesion associated with adenopathy. Ulceroglandular tularemia. Neigh-boring and draining lymph nodes are enlarged, tender, and discrete.
The fluctuation of these nodes occurs later in the illness, after two or more weeks, when other acute signs may have partially abated. Fluctuant buboes four or more weeks old are usu-ally sterile. Generalized lymphadenopathy occurs. Systemic signs of toxemia may be severe in ulcers-glandular tularemia, although most cases are mild or moderate in severity. Occfasvm.a.l.1,3 tularemia referred to as the glandular type may occur as generalized adenopathy and toxemia but without cutaneous lesions. Enteric form of tularemia (typhoidal or crypto-genic). The course of illness may be fulminant and fatal unless the disease is recognized and treated properly. These patients may be severely ill with sustained high fever, profound toxicity, stupor, and delir-ium or coma.
The term “cryptogenic” has often been used to connote the absence of an obvious portal of entry. Pulmonary tularemia. Lung involvement occurs in all forms of tularemia, subsequent to the bacteremia. Available evidence suggests that primary tularemic pneumonia is an entity, particularly in those persons such as laboratory workers who are exposed to infected aerosols. The incubation period varies from two to five days, depending upon the number of viable bacteria inhaled. In
Bacterial Diseases addition to headache, fever, malaise, and prostration, there is a nonproductive harassing cough and a sensation of substernal discomfort. Later the sputum may be mucoid or bloody and, in severely ill patients, there are pleural pain, dyspnea, tachycardia, and cyanosis. In spite of extensive pulmonary involvement, there may be a paucity of physical signs. Which in untreated cases or in those treated late may be prolonged, shadows suggesting abscess formation may be noted. Pleuritis with effusion is not uncommon. Oculoglandular tularemia. Following ocular contamination, there may be pain, photophobia, intense congestion, itching, lacrimation, chemo-sis, and a mucopurulent discharge._ small yellow-ish granulomatous lesions may appear on the palpebral conjunctivae or cornea and may eventually ulcerate.
The preauricular and other regional lymph nodes may enlarge and ultimately suppurate. In untreated patients, serious ocular complications including corneal perforation or optic atrophy may ensue. Other general manifestations. Initially, in severely ill patients, there is a rigor followed by pyrexia that persists for a month or more. Toxic signs in all cases include fever, headache, myalgia, and nausea. Rashes are very uncommon, hen present, they consist of localized papular lesions along the peripheral lymphatics or maculopapular body eruptions.
In untreated patients or in those first given antimicrobial therapy late in the course of illness, convalescence may be prolonged with sporadic episodes of fever, weakness; muscular pains, and chronic respiratory signs. Nonspecific laboratory findings. The erythrocyte sedimentation rate and c-reactive protein are elevated during the active stages. In contrast, the total blood leukocyte count is usually normal' or low. Occasionally there may be moderate leuko-cytosis. Mild albuminuria may occur at the height of illness. Differential diagnosis. Ulceroglandular tularemia is recognized readily in endemic areas. The absence of a rash would favor tularemia because patients with rickettsial disease develop a characteristic exanthem.