Ординатура / Офтальмология / Английские материалы / Basic Sciences in Ophthalmology_Velayutham_2009
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centimeters in diameter and may be visible on chest X-ray. Tissue invasion does not occur. The term allergic bronchopulmonary aspergillosis denotes the condition of patients with preexisting asthma who have eosinophilia, IgE antibody to Aspergillus, and fleeting pulmonary infiltrates from bronchial plugging.
Clinical Manifestations
Endobronchial saprophytic pulmonary aspergillosis presents as chronic productive cough, often with hemoptysis, in a patient with prior chronic lung disease, such as tuberculosis, sarcoidosis, bronchiectasis, or histoplasmosis. Aspergillus may be spread from its endocavitary or endobronchial site to the pleura during the course of bacterial lung abscess or surgery.
Aspergillus sinusitis in immunocompetent patients may take three forms. A ball of hyphae may form in a chronically obstructed paranasal sinus, without tissue invasion. Much less commonly, a chronic, fibrosing granulomatous inflammation associated with Aspergillus hyphae within tissue may begin in the sinus and spread slowly to the orbit and the brain.
Aspergillosis in HIV-infected patients most commonly involves the lung, presenting as fever, cough, and dyspnea. Typically, the CD4 cell count is below 50/uL. Roughly half of these patients have neutropenia or have recently been treated with glucocorticoids.
The growth of Aspergillus on cerumen and detritus within the external auditory canal is termed otomycosis. Trauma to the cornea may cause
Aspergillus keratitis. Endophthalmitis follows the introduction of Aspergillus into the globe by trauma or surgery. Aspergillus may infect intracardiac or intravascular prostheses.
Diagnosis
Culture can be done on Saborauds Dextrose agar with a pH of 5.2, however, Aspergillus spp. can contaminate any basal medium.
Direct Koh examination of the specimen for fungal hyphae. Lactophenol cotton blue stain to see the morphology.
Treatment
Treatment with intravenous Amphotericin B (1.0 to 1.5 mg/kg daily). Itraconazole (200 mg twice daily).
CANDIDIASIS
Candida albicans is the most common cause of mucosal candidiasis and is responsible for about half of all cases of candidemia in hospitalized patients. A small proportion of C. albicans isolates have been transferred to a new
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species, C. dubliniensis. C. tropicalis, C. parapsilosis, C. guilliermondii, C. glabrata (formerly Torulopsis glabrata), C. krusei, and a few other Candida species also cause potentially fatal bloodstream infection. Many of these nonalbicans species can enter the bloodstream through an intravascular catheter. Candida species, taken together, are the fifth most common cause of nosocomial bloodstream infections in the United States.
All Candida species pathogenic for humans are also encountered as commensals of humans, particularly in the mouth, stool, and vagina. These species grow rapidly at 25° to 37°C on simple media as oval, budding cells. In special culture media and in tissue, hyphae or elongated branching structures called pseudohyphae are formed. C. glabrata differs from other members of the genus in that it forms no true hyphae or pseudohyphae in vitro or in infected tissue. C. albicans and C. dubliniensis can be identified presumptively by their ability to form germ tubes in serum or by the formation of thick-walled large spores called chlamydospores (at 25 degree centigrade on corn meal agar). Final identification of all Candida species requires biochemical tests.
Pathogenesis
Candidiasis is often preceded by increased colonization of the mouth, vagina, and stool with Candida due to broad-spectrum antibiotic therapy. Additional local and systemic factors favor infection. Oropharyngeal thrush is particularly likely to occur in neonates and in patients with diabetes mellitus, HIV infection, or dentures. Vulvovaginal candidiasis is especially common in the third trimester of pregnancy. Candida from the perineum can enter the urinary tract via an indwelling bladder catheter. Cutaneous candidiasis most often involves macerated skin, such as that in the diapered area of infants, under pendulous breasts, or on hands constantly in water or covered by occlusive gloves. Candida can pass from the colonized surface into deep tissue when the integrity of the mucosa or skin is violated, as, for example, by perforation of the gastrointestinal tract through trauma, surgery, or peptic ulceration or by mucosal damage due to cytotoxic agents used for cancer chemotherapy. Although Candida is not normally a resident of the skin, secretions from the mouth, rectum, or vagina as well as drainage from surgical wounds or tracheostomy sites can contaminate the hub or skin site of a catheter in an umbilical or central vein. Intravenous drug abuse or third-degree burns can also provide a skin portal for Candida that can lead to deep candidiasis. Once Candida has passed the integumentary barrier, very low birth weight (in neonates) and neutropenia or glucocorticoid therapy (in any patient) markedly compromise host defense. Hematogenous seeding is particularly evident in the retina, kidney, spleen, and liver.
Clinical Manifestations
Oral thrush presents as discrete and confluent adherent white plaques on the oral and pharyngeal mucosa, particularly in the mouth and on the tongue. These
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lesions are usually painless, but fissuring at the corners of the mouth can be painful. Unexplained oropharyngeal thrush raises the possibility of HIV infection. Oral thrush is common in acute HIV infection and becomes increasingly common as the CD4+ cell count falls. At CD4+ counts <50/uL, esophageal thrush also becomes common. HIV infection appears not to be an independent risk factor for vulvovaginal thrush.
Cutaneous candidiasis presents as red macerated intertriginous areas, paronychia, balanitis, or pruritus ani. Candidiasis of the perineal and scrotal skin may be accompanied by discrete pustular lesions on the inner aspects of the thighs. Chronic mucocutaneous candidiasis or candidal granuloma typically presents as circumscribed hyperkeratotic skin lesions, crumbling dystrophic nails, partial alopecia in areas of scalp lesions, and both oral and vaginal thrush.
Esophageal candidiasis is often asymptomatic but can cause substernal pain or a sense of obstruction on swallowing. Most lesions are in the distal third of the esophagus and appear on endoscopy as areas of redness and edema, focal white patches, or ulcers. Biopsy or brushing is required for diagnosis and for detection of concomitant infections, particularly herpes simplex in patients with hematologic malignancies and cytomegalovirus infection inAIDS patients. Esophagography (barium swallow) is diagnostically insensitive but may reveal spasm or mucosal irregularities. Candida esophagitis can cause bleeding and impaired alimentation. Hematogenous dissemination from the esophagus probably occurs in some neutropenic patients but is rarely reported in HIVinfected patients. Candida can cause cystitis and pyelitis.
Hematogenous dissemination can lead to brain abscess or chronic meningitis. Diagnosis of infections of ventriculoperitoneal shunts is difficult because symptoms are indolent and cultures of lumbar fluid are usually sterile.
Diagnosis
Demonstration of pseudohyphae on wet smear with confirmation by culture is the procedure of choice for diagnosing superficial candidiasis. Scrapings for the smear may be obtained from skin, nails, and oral and vaginal mucosa. Culture can be done on Saborauds Dextrose agar. White creamy colonies are formed at 37°C. When the colonies are stained by Gram'
Deeper lesions due to Candida may be diagnosed by histologic section of biopsy specimens or by culture of cerebrospinal fluid, blood, joint fluid, or surgical specimens. Blood cultures are useful in the diagnosis of Candida endocarditis and intravenous catheter-induced sepsis but are positive less often in other forms of disseminated disease. Serologic tests for antibody or antigen are not useful.
Serology is not useful in confirming the infection.
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Treatment
Clotrimazole, miconazole, econazole, ketoconazole, sulconazole, and oxiconazole are available as creams or lotions. Candida vulvovaginitis responds better to an azole than to nystatin suppositories. There is little difference in efficacy among miconazole.
ZYGOMYCOSIS
Zygomycosis (mucormycosis): The clinical entry Zygomycosis, also called mucormycosis is an opportunistic infection often seen in patients with uncontrolled diabetes mellitus.
Morphology: The fungi grow rapidly on all laboratory media not containing cycloheximide. They produce coenocytic hyphae and reproduce sexually by producing sporangia. The sporangiospores develop within sporangia.
Fig. 33.11: Rhizopus species
Etiology: The etiologic agents of most cases of zygomycosis fall into three genera of fungi: Mucor, Rhizopus, Absidia.
Pathogenesis: The infection usually originates in paranasal sinus and involve the ocular orbit and palate extending into the brain. This infection usually occurs as a terminal event in diabetic acidosis and death follows in a few days.
Other clinical forms of zygomycosis are seen in immunocompromized patients, in malnutrition and diarrheal diseases involving lungs, gastrointestinal tract and subcutaneous tissues.
Clinical disease: The lesion present as cotton-like growths on the roof of the mouth or nares in diabetic patients.
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Diagnosis
Diagnosis is usually made clinically and confirmation is made by culture (SDA) and microscopy by KOH examination (non-septate, ribbon-like hyphae) Treatment: Amphotericin B
FUSARIUM (FIG. 33.12)
Several saprophytic fungi such as Fusarium, Aspergillus and Penicillium are occasionally encountered in nail infection usually as secondary invaders following trauma. Fusarium species also produce Keratitis, mycetoma, otomycosis and osteomyelitis following trauma.
Fig. 33.12: Fusarium
Diagnosis
Microscopical examination: The mycelium is septate, conidiospores are single or branching, occasionally producing whorls. The microphialoconidia are single celled and occur in balls. Culture on SDA shows woolly colonies which will turn into orange or violet color later.
PENICILLIUM
Penicillium sometimes produce Keratitis, penicillosis, otomycosis and rarely deep infections.
Morphology: The saprophytic fungi contains septate mycelium and bears flask shaped phial ides, which in turn supports chains of round phial conidia (Fig. 33.13).
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Fig. 33.13: Penicillium in lactophenol stain.
Culture on SDA shows velvety blue green colonies
RHINOSPORIDIOSIS
Rhinosporidiosis is a chronic granulomatous disease caused by agent Rhinisporidium seeberi.
Clinical Features
Rhinosporidiosis is characterized by formation of friable pedunculated or sessile polyp or wart-like lesions in the nasal or nasopharyngeal mucosa, and less often on the conjunctiva of the eye. Rarely other mucosal sites may be affected.
The mode of infection and transmission are not known but most infections occur in males with frequent contact with stagnant water or aquatic life.
Diagnosis
The fungus has not been cultivated. Laboratory diagnosis is made by demonstration of sporangia in tissues (HPE)
Fig. 33.14: Histopathology showing sporangiospores
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DIMORPHIC FUNGI
Dimorphic fungi are fungi that grow as filamentous mould at 25 degree centigrade and transform to unicellular yeast in tissue and culture at 37 degree centigrade.
There are five types of dimorphic fungi:
1.Histoplasma capsulatum
2.Blastomyces dermatitidis
3.Coccidioides immitis
4.Paracoccidioides braziliensis
5.Cryptococcus neoformans
HISTOPLASMA CAPSULATUM
Etiologic Agent
Histoplasma capsulatum is a dimorphic fungus that grows as a mold in nature or on Sabouraud's agar at room temperature (Fig. 33.15). Hyphae bear both large and small spores, which are used for identification. Nucleic acid hybridization can also be used to identify the organism in culture. H. capsulatum grows as a small budding yeast in host tissue and on enriched agar, such as blood cysteine glucose, at 37°C. Despite its name, the fungus is unencapsulated. Coculture of isolates with opposite mating types can produce different sporulating structures in which genetic recombination occurs. When these structures, referred to as a teleomorph or the perfect state, are seen in culture, the name Ajellomyces capsulatus is used.
Fig. 33.15: Histoplasma capsulatum
Infection with H. capsulatum has been encountered in many areas of the world but is much more frequent in certain areas. Within the United States, infection is most common in the southeastern, mid-Atlantic, and central states.
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Pathogenesis
Microconidia, or small spores, of H. capsulatum are small enough to reach the alveoli on inhalation and are transformed there to budding forms. With time, an intense granulomatous reaction occurs. Caseation necrosis or calcification may mimic tuberculosis. In children, the primary infection usually heals completely but may leave spotty calcification in the hilar nodes or lung. Transient dissemination may leave calcified granulomas in the spleen. In adults, a rounded mass of scar tissue, with or without central calcification, may remain in the lung. This mass has been called a histoplasmoma. Previous exposure is thought to confer some protection against reinfection, but infection in persons with prior positive skin tests clearly has occurred.
Clinical Manifestations
The vast majority of infections are either asymptomatic or mild, and the diagnosis is elusive. Cough, fever, malaise, and chest X-ray findings of hilar adenopathy with or without one or more areas of pneumonitis are typical features. Erythema nodosum and erythema multiforme have been reported in a few outbreaks.
Chronic pulmonary histoplasmosis is characterized by a gradual onset (over weeks or months) of increasing productive cough, weight loss, and sometimes night sweats. Chest X-ray reveals unior bilateral fibronodular apical infiltrates.
Diagnosis
Culture of the etiologic organism is the preferred method for diagnosis of histoplasmosis but is often difficult. Blood cultures are best done by the lysiscentrifugation technique, with plates held at 30°C for at least 2 weeks. Approximately 15 mL of blood should be cultured. Diagnosis based on Giemsastained smears of blood or bronchoalveolar lavage fluid or on methenamine silver staining of infected tissue. Neither skin testing nor serology has been predictive of histoplasmosis in patients infected with HIV.
Treatment
Itraconazole (200 mg/d), Fluconazole, Ketoconazole (400 to 800 mg once daily) and amphotericin B (0.6 mg/kg daily).
BLASTOMYCOSIS
Blastomyces dermatitidis is a dimorphic fungus that grows at room temperature as a white or tan mold but grows within the host or at 37°C as budding, round yeastlike cells. The fungus can be identified on the basis of its appearance, its dimorphism, the small spores borne on hyphae of the mold form, or the results
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of nucleic acid hybridization. When isolates of the two opposite mating types are grown close together on special culture medium, such as yeast extract or soil extract agar, sporulating structures that characterize the perfect state (teleomorph), called Ajellomyces dermatitidis, appear.
Pathogenesis
Infection with B. dermatitidis appears to be acquired by inhalation of the fungus from soil, decomposed vegetation, or rotting wood. Several case clusters have resulted from participation in recreational activities in wooded areas along waterways. Infection is not transmissible from person to person. The initial pulmonary infection may either heal spontaneously or become chronic. Spread to other portions of the lung, cavitation, or endobronchial lesions may be found in patients with chronic disease.
Clinical Manifestations
A few patients have acute, self-limited pneumonia. Fever, productive cough, myalgia, and malaise usually resolve within a month. Pulmonary infiltrates clear slowly as B. dermatitidis disappears from the sputum.
In the vast majority of patients, blastomycosis has an indolent onset and a chronically progressive course. Fever, cough, weight loss, lassitude, skin lesions, and chest ache are common. Skin lesions favor exposed areas and enlarge over many weeks from pimples to well-circumscribed, verrucous, crusted, or ulcerated lesions. Pain and regional lymphadenopathy are minimal. Large chronic lesions may undergo central healing with scarring and contracture. Mucous membrane lesions resemble squamous cell carcinoma. Chest X-ray findings are abnormal in two-thirds of patients, with one or more pneumonic or nodular infiltrates. Calcification, hilar adenopathy, and large pleural effusions are rare. Osteolytic lesions may be found in nearly any bone and present as a cold abscess or a draining sinus. Extension to a contiguous joint may cause indolent swelling, pain, and restricted motion. Prostatic and epididymal lesions clinically resemble those of tuberculosis.
Diagnosis
The diagnosis of blastomycosis is made by demonstration of the fungus in a culture of sputum, pus, or urine. An expert can diagnose blastomycosis on the basis of the appearance of the organism in wet smear or histopathologic section. The fungus may be visible in a sputum cytology smear but is easily overlooked.
Treatment
Intravenous amphotericin B, itraconazole (200 mg twice daily with food).
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COCCIDIOIDOMYCOSIS
Coccidioides immitis has two forms, growing as a white fluffy mold on most culture media but as a non-budding spherical form (a spherule) in host tissue or under special condition. The organism reproduces in host tissue by forming small endospores within mature spherules. After rupture of the spherule, the released endospores enlarge, become spherules, and repeat the cycle. The fungus is identified by its appearance and by the formation of thick-walled, barrel-shaped spores, called arthrospores, in the hyphae of the mold form (Fig. 33.16).
Pathogenesis
C. immitis is a soil saprophyte found in certain arid regions of the United States, Mexico, Central America, and South America. Within the United States, most cases of infection with C. immitis are acquired in California, Arizona, and western Texas. A few cases are acquired by exposure to fomites from endemic areas (e.g. in cotton bales).
Infection in humans and animals results from inhalation of wind-borne arthrospores from soil sites. This primary pulmonary infection is symptomatic in only 40% of cases, with symptoms ranging from a mild influenza-like illness to severe pneumonia. Mild self-limited infections may come to medical attention because of case clusters or hypersensitivity reactions: erythema nodosum, erythema multiforme, toxic erythema, arthralgia, arthritis, conjunctivitis, or episcleritis.
Pleural effusion may be the only manifestation of primary infection. Spontaneous healing of this form is common.
Fig. 33.16: Arthospores of Coccidioides immitis