Chapter 139. Haemophilus Infections (Kỳ 5)

Clinical ManifestationsInfection is acquired as the result of a break in the epithelium during sexual contact with an infected individual. After an incubation period of 4–7 days, the initial lesion—a papule with surrounding erythema—appears. In 2 or 3 days, the papule evolves into a pustule, which spontaneously ruptures and forms a sharply circumscribed ulcer that is generally not indurated (Fig. 139-2). The ulcers are painful and bleed easily; little or no inflammation of the surrounding skin is evident. Approximately half of patients develop enlarged, tender inguinal lymph nodes, which frequently become fluctuant and spontaneously rupture. Patients usually seek medical...
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Chapter 139. Haemophilus Infections (Kỳ 5) Chapter 139. Haemophilus Infections (Kỳ 5) Clinical Manifestations Infection is acquired as the result of a break in the epithelium during sexualcontact with an infected individual. After an incubation period of 4–7 days, theinitial lesion—a papule with surrounding erythema—appears. In 2 or 3 days, thepapule evolves into a pustule, which spontaneously ruptures and forms a sharplycircumscribed ulcer that is generally not indurated (Fig. 139-2). The ulcers arepainful and bleed easily; little or no inflammation of the surrounding skin isevident. Approximately half of patients develop enlarged, tender inguinal lymphnodes, which frequently become fluctuant and spontaneously rupture. Patientsusually seek medical care after 1–3 weeks of painful symptoms. The presentation of chancroid does not usually include all of the typicalclinical features and is sometimes atypical. Multiple ulcers can coalesce to formgiant ulcers. Ulcers can appear and then resolve, with inguinal adenitis (Fig. 139-2) and suppuration following 1–3 weeks later; this clinical picture can be confusedwith that of lymphogranuloma venereum (Chap. 169). Multiple small ulcers canresemble folliculitis. Other differential diagnostic considerations include thevarious infections causing genital ulceration, such as primary syphilis, condylomalatum of secondary syphilis, genital herpes, and donovanosis. In rare caseschancroid lesions become secondarily infected with bacteria; the result isextensive inflammation. Diagnosis Clinical diagnosis of chancroid is often inaccurate, and laboratoryconfirmation should be attempted in suspected cases. Grams staining of a swab ofthe lesion may reveal a predominance of characteristic gram-negative coccobacilli,but the presence of other bacteria often makes it difficult to interpret this result.An accurate diagnosis of chancroid relies on culture of H. ducreyi from the lesion.In addition, aspiration and culture of suppurative lymph nodes should beconsidered. Since the organism can be difficult to grow, the use of selective andsupplemented media is necessary. A multiplex polymerase chain reaction assayhas been developed for simultaneous amplification of DNA targets from H.ducreyi, Treponema pallidum, and herpes simplex virus types 1 and 2. When thisassay becomes commercially available, it will be a useful diagnostic tool withwhich to identify the etiology of genital ulcers. Haemophilus ducreyi: Treatment The treatment regimen recommended by the Centers for Disease Controland Prevention is a single 1-g oral dose of azithromycin. Alternative regimensinclude ceftriaxone (250 mg intramuscularly in a single dose), ciprofloxacin (500mg orally bid for 3 days), or erythromycin base (500 mg orally tid for 7 days).Isolates from patients who do not respond promptly to treatment should be testedfor antimicrobial susceptibility. In patients with HIV infection, healing may beslow and longer courses of treatment may be necessary. Clinical treatment failurein HIV-seropositive patients may reflect co-infection, especially with herpessimplex virus. Contacts of patients with chancroid should be identified and treated,whether or not symptoms are present, if they had sexual contact with the patientduring the 10 days preceding the patients onset of symptoms. Further Readings Bong CT et al: Haemophilus ducreyi: Clinical features, epidemiology, andprospects for disease control. Microbes Infect 4:1141, 2002 [PMID: 12361914] Casey JR, Pichichero ME: Changes in frequency and pathogens causingacute otitis media in 1995–2003. Pediatr Infect Dis J 23:824, 2004 [PMID:15361720] Committee on Infectious Diseases: Haemophilus influenzae infections, in2003 Red Book, Report of the Committee on Infectious Diseases, 26th ed, LKPickering et al (eds). Elk Grove Village, IL, American Academy of Pediatrics,2003 Dominguez SR, Daum RS: Toward global Haemophilus influenzae type bimmunization. Clin Infect Dis 37:1600, 2003 [PMID: 14689338] Heilmann KP et al: Decreasing prevalence of beta-lactamase productionamong respiratory tract isolates of Haemophilus influenzae in the United States.Antimicrob Agents Chemother 49:2561, 2005 [PMID: 15917574] Kelly DF et al: Haemophilus influenzae type b conjugate vaccines.Immunology 113:163, 2004 [PMID: 15379976] Liebowitz E et al: Haemophilus influenzae: A significant pathogen in acuteotitis media. Pediatr Infect Dis J 23:1142, 2004 McGillivary G et al: Cloning and sequencing of a genomic island found inthe Brazilian purpuric fever clone of Haemophilus influenzae biogroup aegyptius.Infect Immun 73:1927, 2005 [PMID: 15784532] Murphy TF: Respiratory inf ...