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Review
. 2006 Apr;37(4):381-90.
doi: 10.1016/j.humpath.2006.01.015.

The comparative pathology of severe acute respiratory syndrome and avian influenza A subtype H5N1--a review

Wai-Fu Ng  1 , Ka-Fai To, William W L Lam, Tak-Keung Ng, Kam-Cheong Lee
Affiliations
Review

The comparative pathology of severe acute respiratory syndrome and avian influenza A subtype H5N1--a review

Wai-Fu Ng et al. Hum Pathol. 2006 Apr.

Abstract

The pathology of 2 zoonotic human viral infections that recently emerged, severe acute respiratory syndrome (SARS) due to coronavirus (SARS-CoV) and avian influenza A subtype H5N1, is reviewed and compared based on the literature and the cases examined by the authors. Pneumocytes are the primary target of infection resulting in diffuse alveolar damage. Systemic cytokine activation results in hemophagocytic syndrome, lymphoid depletion, and skeletal muscle fiber necrosis. Severe acute respiratory syndrome induces a more fibrocellular intra-alveolar organization with a "bronchiolitis obliterans organizing pneumonia"-like pattern and presence of multinucleated histiocytes and pneumocytes. H5N1 causes a more fulminant and necrotizing diffuse alveolar damage with patchy and interstitial paucicellular fibrosis. Severe acute respiratory syndrome associated coronavirus persists in the lung up to the second month, whereas H5N1 persists in the lung up to the third week. Severe acute respiratory syndrome associated coronavirus disseminates to blood, urine, feces, gastrointestinal tract, and liver. There is recent report of possible cerebral involvement by H5N1 and its isolation in the blood, gastrointestinal tract, and cerebrospinal fluid. More pathologic studies are urgently needed.

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Figures

Fig. 1
Fig. 1
Pulmonary pathology of SARS. A, Acute exudative DAD with hyaline membrane. B, Mixed inflammatory cells exudative in acute DAD. C, Organizing DAD with intra-alveolar fibrocellular infiltrate. Note a histiocytic giant cell in upper part of the field. D, BOOP-like pattern of organization. E1, Multinucleated pneumocyte. E2, Multinucleated histiocyte labeled with the histiocytic marker CD68. F, Pneumocytic regeneration labeled by the epithelial marker AE1/AE3 (hematoxylin-eosin stain unless specified, original magnification ×630 [B], ×1000 [E1], ×400 [E2], and ×100 [all others]; E1 taken from a patient with SARS dying on day 18, all others taken from a patient with SARS dying on day 20).
Fig. 2
Fig. 2
Extrapulmonary pathology of SARS. A, Reactive hemophagocytosis in pulmonary hilar lymph node. B, Reactive hemophagocytosis in bone marrow. C, Lymphoid depletion in spleen. D, Skeletal muscle fiber necrosis. E, Acute tubular necrosis of kidney compared with normal tubule at left upper corner. F, Mitosis and apoptosis of hepatocytes (arrowheads) and ballooning degeneration in SARS-CoV–associated hepatitis (hematoxylin-eosin stain, original magnification ×1000 [A and B] and ×400 [all others]; A and B taken from a patient with SARS dying on day 18; C-E taken from a patient with SARS dying on day 20; F taken from liver biopsy of a patient with SARS on day 31).
Fig. 3
Fig. 3
Pulmonary pathology of H5N1. A, Acute exudative DAD with hyaline membrane. B, Necrotizing and hemorrhagic area of DAD. C, Mixed inflammatory cell exudates in acute DAD labeled with the histiocytic marker CD68. Note the strongly reactive histiocytic cells, weakly reactive neutrophils, and unreactive lymphocytes (D, E). Organizing DAD with interstitial hyaline and paucicellular fibrosis. F, Pneumocytic hyperplasia labeled by the epithelial marker AE1/AE3. Note area of alveolar destruction with patchy and interstitial fibrosis (hematoxylin-eosin stain unless specified, original magnification ×630 [2C], ×200 [2E], and ×100 [all others]; A-C taken from a patient with H5N1 dying on day 10 [case 3 of Table 2]; D-F taken from a patient with H5N1 dying on day 30 [case 1 of Table 2]).
Fig. 4
Fig. 4
Extrapulmonary pathology of H5N1. A, Reactive hemophagocytosis in pulmonary hilar lymph node and 3 large activated lymphocytes in the center of field. B, Reactive hemophagocytosis in bone marrow. C, Lymphoid depletion in spleen and large activated lymphocytes in inset. D, Skeletal muscle fiber necrosis. E, Microglial nodules with rarefaction and demyelination in cerebral white matter. F, High-power view of microglial nodule with a few axon balls in the lower field and foamy and pigment-laden macrophages (hematoxylin-eosin stain, original magnification ×1000 [A, B, and C inset], ×100 [4E], ×400 [all others]; A-D taken from a patient with H5N1 dying on day 10 [case 3 of Table 2]; E and F taken from a patient with H5N1 dying on day 30 [case 1 of Table 2]).
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