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Typhoidal tularemia refers to a febrile illness caused by F. tularensis unassociated with prominent lymphadenopathy and not fitting into any of the other primary forms.
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The typhoidal form may result from any mode of acquisition, and it is the most difficult to diagnose.
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Because the portal of entry is usually inapparent clinically, a history of outdoor activities with tick, insect, or animal exposure should be pursued.
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Many patients have underlying severe chronic medical disorders and their presentation can be dramatic, with acute prostration and rapid death, or protracted illness
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The examination may reveal dehydration, hypotension, mild pharyngitis and cervical adenopathy, meningismus, and diffuse abdominal tenderness. Hepato- megaly and splenomegaly are found uncommonly in the acute stages and become more likely the longer the duration of illness.
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Prominent symptoms of typhoidal tularemia may include any combination of fever with chills, headache, myalgia, sore throat, anorexia, nausea, vomiting, diarrhea, abdominal pain, and cough.
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Severe disease may cause jaundice produced by cholestasis
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Diarrhea is a major manifestation only in typhoidal tularemia. Bowel movements are loose and watery but only rarely bloody. Children may have more severe intestinal involvement, including focal areas of bowel necrosis.161
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Rare gastrointestinal manifestations include cholangitis, granulomatous hepatitis, and liver abscess
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Secondary pleuropulmonary involvement is fairly frequent in this form. Pulmonary infiltrates, pleural effusions, or even pulmonary nodules are described in up to 45% of subacute to chronic typhoidal cases173,174,175; it is even more frequent in laboratory-acquired infections.
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Additional findings in severely ill patients may include hyponatremia, elevated creatine phosphokinase level, myoglobinuria, pyuria, renal failure, and positive blood cultures.
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The differential diagnosis of typhoidal tularemia would be extensive and includes typhoid fever caused by Salmonella spp., brucellosis, Legionella infection, Q fever, disseminated mycobacterial or fungal infection, rickettsioses, malaria, endocarditis, and any other cause of prolonged fever without localizing signs
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Pneumonic tularemia was the primary clinical presentation in 39% of adults and 24% of patients overall among classifiable cases reported in Missouri between 2000 and 2007, and as common as ulceroglandular disease in Colorado, Nebraska, South Dakota, and Wyoming during 2015 when the number of reported tularemia cases in these states significantly increased.88,163
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It may result from direct inhalation of the organism or secondary hematogenous spread to the lung
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Primary pneumonic tularemia is a risk for certain occupations, including sheep shearers, farmers, landscapers, and laboratory workers.
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Cases also have been described as resulting from common exposure in a more casual setting, such as a converted mill building for holiday stays.177 This case was linked to infected dog dander exposure, as was a recent case in a patient with sarcoidosis who had no other likely exposure.115
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Pneumonia with F. tularensis subsp. holarctica bacteremia also has been described after freshwater near drowning.178
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Secondary pneumonia may occur early or after a delay of weeks to months in the course of tularemia.3
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Although secondary pneumonia may complicate any of the syndromes already discussed, Evans and colleagues160 found pneumonia to be most frequent in typhoidal (83%) and ulceroglandular (31%) diseases.
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Scofield and associates179 reported that patients with pneumonic involvement were more likely to be older, recall no exposure risk, present with typhoidal illness, have positive cultures, stay hospitalized longer, and have a higher mortality rate.
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From 25% to 30% of patients have infiltrates on radio- graphic examination without any clinical findings of pneumonia.160
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A series of 58 patients with pulmonary tularemia in Finland found 47% lacking respiratory symptoms and 7% having a normal chest radiograph, though variable findings of chest computed tomography secured a pneumonic designation.180
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Pneumonia from F. tul ar e ns i s subsp. tularensis is typically a more severe disease than that caused by F. tul are nsi s subsp. holarctica, but pneumonia caused by F. tu la re nsi s subsp. holarctica may be severe in immunocompromised patients.181 The illness may be prolonged with either subspecies
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Common symptoms include fever, cough, no or minimal sputum production, substernal tightness, and pleuritic chest pain.109 Hemoptysis may occur but is uncommon.
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Physical examination may be nonspecific or may reveal rales, consolidation, and a friction rub or signs of effusion
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Routine examination of sputum does not help to suggest the diagnosis. However, a false-positive DFA stain for Legionella on bronchoscopy specimens has been reported and may be easily confused with Legionella pneu- monia.182,183
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Infected pleural fluid is exudative and negative on Gram stain, and usually contains more than 1000 leukocytes/mm3; cells are predominantly lymphocytes, but neutrophilic effusions may occur.
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Pleural effusions seen with tularemia frequently mimic those of tuber- culosis. Similar findings for both include a lymphocyte-rich exudative pleural effusion and a high adenosine deaminase concentration.184 Granulomas may be found on pleural biopsy, prompting understandable confusion with tuberculosis
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Acute radiographic changes may include subsegmental or lobar infiltrates (Fig. 227.5), hilar adenopathy, pleural effusion, and apical or miliary infiltrates; less common changes include ovoid densities, cavitation, and bronchopleural fistula. However, in some patients the initial chest radiographs are normal.
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Secondary pneumonias are more likely to involve the lower lobes and be bilateral, perhaps because of their hematogenous origin.
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Healing usually occurs without residual changes, but fibrosis and calcifications may result. Therefore tularemia may manifest as enigmatic community-acquired pneumonia that does not respond to routine therapies.
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The differential diagnosis of pneumonic tularemia includes Mycoplasma pneumonia, Legionella infection, Chlamydia pneumoniae infection, Q fever, psittacosis, tuberculosis, the deep mycoses, and many other causes of atypical or chronic pneumonias
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Patients in four consecutive cases of pneumonic tularemia reported from Switzerland presented with fever of 1 to 8 weeks’ duration and were found to have one or more dense nodular pulmonary infiltrates suspicious of cancer and hilar or mediastinal lymphadenopathy.173 18F-Fluorodeoxyglucose–positron emission tomography/computed tomography scans were highly positive in all four patients. Diagnosis was suspected by finding necrotizing granulomas in the nodes by using transbronchial needle aspiration or thoracoscopy. Node tissue was PCR positive for F. tu l ar e n si s in three patients; subspecies were not determined.

Tularemia agglutination titers were positive in all cases, with titers of 1 : 320 to 1 : 5120. Three patients responded to ciprofloxacin. One relapsed after doxycycline and responded to gentamicin plus ciprofloxacin. A similar patient from France also responded to ciprofloxacin.

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Primary skin rashes due to tularemia have been described, including on the face and elsewhere.186
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Secondary rashes are an underappreciated part of tularemia and may be found in up to 52% of cases, especially with oropharyngeal presentations.159,187,188,189 They usually appear within the first 2 weeks of symptoms, but in a minority of cases they are delayed.
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The rash is more common in women than in men.
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Cutaneous changes may include diffuse maculopapular and vesiculopapular erup- tions, pustules, erythema nodosum, erythema multiforme, acneiform lesions, and urticarial and vasculitis-like eruptions.189 Sweet syndrome has also been reported in association with tularemia.190
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Although any secondary rash may be part of any form of tularemia, erythema nodosum has been found to occur most commonly with pneumonic tularemia, while erythema multiforme was described in 11.3% of patients in a large Turkish series, most of whom presented with oropharyngeal or glandular forms.191
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These worldwide reports and the molecular identification of older F. tul ar ensi s isolates as F. tu la re n si s subsp. novicida after being previously classified as other subspecies suggest that infections caused by F. tularensis subsp. novicida may be underappreciated
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An outbreak of three symptomatic cases of F. tu lar ens is subsp. novicida bacteremia occurred in a Louisiana prison, and one patient died.96 F. tu lar ensi s subsp. novicida was isolated from one of the facility ice machines, believed to be the most likely vehicle for its transmission
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Brett and coworkers193 identified F. tularen si s subsp. novicida bacteremia in a patient who nearly drowned while body surfing along the South Carolina coast.193
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The clinical manifestations of infections caused by F. tularensis subsp. novicida are less well characterized than for the other subspecies.
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F. philomiragia infection has caused a skin vesicle, pneumonia, empyema, sepsis, peritonitis, splenic microabscesses, and meningitis. This organism predominantly infects patients with host defenses impaired by chronic granulomatous disease, near drowning in salt water or estuaries, myeloproliferative disorders, or renal transplantation.194,195,196 Only a small number of cases have been documented, more from North America than Europe, and the organism has been found in tissues, blood, cerebrospinal fluid, and other body fluids.
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The 2001 Tularemia Consensus Statement developed by the Working Group on Civilian Biodefense concluded that aerosolization would be the most likely method for dispersing F. tularensis, because inhalation of bacilli would affect the highest number of people with the most devastating manifestations of the disease.197
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Children are theorized to be more vulnerable than adults to an aerosolized agent because of their higher respiratory rate, more permeable skin, and higher skin-to-mass ratio.198 Secondary cases may also arise following contact with contami- nated environmental sources or animals.199
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Bioterrorisme
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After an aerosol release and an incubation period of 3 to 5 days, patients may present with the acute onset of fever (38°–40°C [100.4°–104°F]), malaise, headache, rigors, coryza, and sore throat. The subsequent clinical syndrome depends on the immune status of the host, the inhaled inoculum, and the virulence of the released agent
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Bioterrorisme
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Because airborne organisms also may invade through extrapulmonary sites and food and water may be contaminated, less common presentations could include oculoglandular, pharyngeal, ulceroglandular, or glandular disease.200
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Bioterrorisme
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It is anticipated that most patients would develop either primary pneumonic or typhoidal forms.197 A significant number of patients may develop respiratory failure or have signs and symptoms heralding severe sepsis.
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Bioterrorisme
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Rapid recognition and reporting of a possible bioterrorist event due to tularemia is a difficult clinical challenge. It should be suggested by clustered cases of pneumonic or typhoidal disease, particularly in urban areas in patients without the usual exposure history
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