Pulmonary Fungal Infections 2 Flashcards
cryptococcosis organisms
5 serotypes: A, D, and AD are neoformans. B and C are gattii. Neoformans is environmental, found worldwide in soil contaminated with bird droppings. Gattii is found under eucalyptus trees. Oval yeasts with narrow based buds and wide polysaccharide capsule. pathogenic strains grow at 37C. not thermally dimorphic, but does have a moldlike sexually reproducing form (filobasidiella). no human to human transmission except organ transplant or needle sticks.
cryptooccosis pathogenesis
transmitted by inhalation. lung infection may be asymptomatic or lead to pneumonia. can be intracellular infection through alveolar macrophages. immunocompetent restrict infection to lungs. successful hosts raise helper Ts, skin test conversion, antibodies to the capsule. dissemination leads to meningitis w/ skin nodules. Neoformans raises little inflamm response, damages by distorting tissue through growing yeast.
cryptococcosis virulence factors
capsule, melanin in cell wall (antiphagocytic), phospholipase B for invading tissue
cryptococcosis exam
history of steroid use, malignant disease, transplantation, HIV infection. Skin: take biopsies of nodules. Meningitis symptoms if CNS is affected. Cryptococcomas can cause focal neurologic defects. blunted inflammatory response complicates diagnosis and means that presentation is late in disease
cryptococcosis lab
CSF: stain with india ink to see yeast. Biopsies: stain with silver or schiff. Culture at 37C from CSF, blood, urine, sputum. cultures produce melanin. serology: crag latex agglutination for cryptococcal antigen in blood and CSF. routine bloodwork may be normal
cryptococcosis treatment
meningitis or cryptococcoma: amphotericin B plus flucytosine followed by fluconazole.
Prostate: fluconazole
Skin, bones, other: amphotericin B
aspergillosis organisms
Aspergillus fumigatus, niger, flavus, clavatus. ubiquitous environmental molds. only mold, not dimorphic. septate hyphae with V- shaped branhes. walls are nearly parallel, conidia form radiating changes
4 syndromes caused by aspergillosis
- allergic bronchopulmonary aspergillosis
- aspergilloma or colonizing aspergilliosis (fungal ball in lung)
- chronic necrotizing pulmonary aspergillosis
- invasive aspergillosis
aspergillosis pathogenesis
widespread on decaying vegetation. infectious conidia are airborne. ABPA is hypersensitivity reaction to infection of bronchi by aspergillus. aspergilloma has balls that form when aspergillus invades cavitary lesions of TB or CF. CNPA are granulomas that form in immunocompromised. Invasive aspergillosis is a rapidly progressive invasion of blood vessels in severely immunosuppressed patients, involves infarction, hemorrhage, necrosis, often fatal.
aspergillus virulence factors
gliotoxin: immunosuppressive. toxic metabolites interfere with phagocytosis and opsonization. proteases may be involved in tissue invasion.
ABPA exam
positive skin test for aspergillus allergy with asthma or CF. coughing up brownish bronchial plugs containing hyphae. fever, wheezing, pulmonary infiltrates unresponsive to antibiotics. Xray/CT may show grape cluster or hand in mitten clusters of bronchi
aspergilloma/colonizing aspergilliosis exam
fungal ball visible on xray or CT. doesnt invade tissue but may cause dangerous hemoptysis. cough, fever.
CNPA exam
subacute pneumonia unresponsive to antibiotics. underlying disease of alcoholism, collagen-vascular disease, chronic granulomatous disease or COPD. longterm corticosteroid therapy. fever, cough, night sweats, weight loss. history of ineffective treatment for TB. needle biopsy, aspirate fluid if present
invasive aspergillosis
history of profound immunosuppression or COPD with long term corticosteroid therapy. fever, cough, dyspnea, pleuritic chest pain, neutropenia, sometimes hemoptysis, worsening hypoxemia. CT scan may show halo sign: ground glass infiltrate surrounding a nodular density. do biopsy of lung
aspergillosis lab
cultures from sputum, needle biopsy, or bronchoalveolar lavage fluid. visualize with silver stains, colonies with radiating chains of conidia. grows fast. invasive shows septate hyphae at acute angles, tissue necrosis, blood vessel invasion. ABPA shows high levels of IgE and eosinophilia, along with mucus with hyphae
aspergillosis treatment
ABPA: oral corticosteroids and itraconazole.
Aspergilloma: remove surgically if hemoptysis, oral itraconazole
Invasive or CNPA: voriconazole and ampho B. decrease immunosuppression if possible. surgical resection of diseased area.
mucormycosis organisms
rhizopus, mucor, absidia, and others. rare sinus infections. widespread environmental. not dimorphic. risk factors include diabetes, neutropenia. must treat underlying disease and add amphotericin B
mucormycosis pathogenesis
transmitted by airborne asexual spores. ubiquitous worldwide. cause disease in vulnerable patients. usually inhaled. invade tissues of patient with immunosuppression. neutrophils are main host defense. not highly associated with AIDS. mainly hit paranasal sinuses, lungs, gut, skin, or disseminated. cause infarction and necrosis of tissue downstream from blocked vessel.
mucormycosis exam
symptoms at affected site. rhinocerebral shows unilateral retro-orbital headache, face pain, numbness, fever. progresses to diplopia and visual loss, loss of consciousness etc. wound infections unresponsive to antibiotics. Lung and GI are nonspecific, biopsy useful. Cutaneous: cellulitis progressing to dermal necrosis and black eschar formation
mucormycosis lab
bloodwork: neutropenia, diabetic acidosis, iron overload. no useful antigen tests or CSF. biopsy shows nonseptate hyphae branching at right angles. culture is difficult.
mucormycosis treatment
send to tertiary care facility. change any pre-existing bandages/splints. if early diagnosis, treat with amphotericin B and aggressive surgical removal of necrotic tissue. surgery needed.
fusarium mycology
fusarium species are environmentally ubiquitous. identified microscopically by a banana shaped macroconidia. primarily pathogens of plants, including important crops. Solani is most common.
fusarium virulence factors
immunosuppressive mycotoxins. collagenases and proteases. ability to adhere to prosthetic material.
mycotoxicosis pathogenesis
trichothecene mycotoxins -> alimentary toxic aleukia. widespread bleeding and immunosuppression with secondary sepsis, often fatal. yellow rain
immunocompetent local infection of fusarium
skin, cornea, allergic sinusitis, colonization of prosthetics and catheters. treat with amphotericin B, voriconazole, posaconazole.
immunosuppressed opportunistic infection of fusarium
prolonged neutropenia. long term use of steroids. profound T cell deficiency.
disseminated infection of fusarium
usually invades from sinus or at a wound site. presents as fungemia with skin lesions. may also seed eye, lung, cause local symptoms there.
fusarium diagnosis
grows easily on fungal media, but is ubiquitous. need multiple samples and sites. histology can only differentiate from aspergillus if yeast form is present along with the acute branching hyphae. PCR-based tests and fungal metabolism tests are available.
fusarium treatment
more resistant to antifungals than the other pathogenic fungi. surgical excision. try amphotericin B with natamycin or voriconazole. prognosis in disseminated is poor.
fusarium prevention
keep high risk patients in a HEPA filtered room at positive pressure. pre-op workup must include screening for fusarial infection, as it could be bad after you get immunosuppressed.
