Disseminated parasitosis in an immunosuppressed patient. Possibly a mutated sparganum.

The autopsy of a man who died of Hodgkin disease revealed that a peculiar metazoan parasite had proliferated and disseminated throughout his body. The parasite could not be identified; however, electron microscopical studies revealed that it had the structure of a flatworm. This, together with its shape and structure, convinced us that the parasite was an aberrant sparganum manifesting uncontrolled proliferation and dissemination.

Recovery of reovirus type 2 from an immature dog with respiratory tract disease.

Two similar cytopathic agents were recovered from the throat and rectal swab specimens of an immature dog with upper respiratory tract disease. The reference isolate, 14-72R, was shown to be a member of the reovirus group by its physicochemical properties, cytopathic effects in cell cultures, and appearance when examined in the electron microscope. Both isolates hemagglutinated human type O erythrocytes and antigenically were closely related to reovirus type 2. The affected pup had an increase in antibody titer to reovirus types 2 and 3. The latter findings provide evidence for possible heterotypic antibody responses in dogs to reovirus infection.

Light microscopy of selected viral diseases (morphology of viral inclusion bodies).

A significant number of viruses produce intracellular changes, inclusion bodies, which do have specific and consistent features important to their identification. The inclusions must fulfill the designated criteria for the specific virus or a member of that group. The specific features of viral inclusions are consistent fixative-dependent artifacts: uniformity and familiarity of staining quality are important to the consistency of recognition and identification. Bouin's or Zenker's-acetic acid are the fixatives of choice, and a well-done hematoxylin and eosin stain offers the greatest uniformity of quality. Viral inclusions are not static objects in a cell and recognition of the range of development is often more important than the appearance of a single inclusion. Generally, most viruses within a group cause identical intracellular reactions and produce similar inclusion bodies, thus permitting the pathologist an accurate prediction of the etiologic agent in clinically undiagnosed or unsuspected viral disease. By correlating viral inclusion identification, clinical history, and physical findings the anatomic pathologist can make the diagnosis of many viral diseases rapidly, inexpensively, and with a high degree of accuracy when compared to the complex, expensive, and time consuming procedures of animal inoculation, tissue culture, or serology.

Mouse cytomegalovirus. Necrosis of infected and morphologically normal submaxillary gland acinar cells during termination of chronic infection.

The ultrastructural lesions in the submaxillary glands of C(3)H mice chronically infected with the murine cytomegalovirus are reported. Virus was synthesized in the nucleus of acinar glandular cells. After passage into the cytoplasm, virus was located in large vesicles which were derived from the Golgi apparatus. These vesicles, which were periodic acid-Schiff positive, migrated to the apex of the cell and released virus into the acinar lumen or canaliculi. Eventually, lymphocytes infiltrated the interstitium and surrounded the basal lamina of acini which contained infected cells. In acini encompassed by lymphocytes, both infected cells and morphologically normal acinar cells simultaneously degenerated, producing a small focus of necrosis. Physical contact between lymphocytes and necrotic cells did not occur for an intact basal lamina was always found interposed between them. Degeneration of infected cells coincided with a decrease in virus titer in the salivary glands. Degeneration of infected and normal acinar cells also occurred in DBA 2 mice which lack the fifth component of complement. In mice conditioned with cortisone to suppress inflammation, neither infected nor normal acinar cells degenerated. We concluded from the electron microscope observations that lymphocytes terminate chronic MCMV infection, that MCMV infection of acinar epithelium is not cytolytic and that normal cells also undergo necrosis during termination of chronic MCMV infection. It is postulated that lymphocytes in responding to infection release a cytotoxic substance which diffuses into the acini and causes indiscriminate necrosis of acinar cells.

Methotrexate-induced sudden fatal pulmonary reaction.

A teenage girl in bone marrow remission with acute lymphocytic leukemia died suddenly from pulmonary edema. She had taken her first oral dose of methotrexate and cyclophosphamide 10 hours previously when she was feeling well and was asymptomatic. One week previously she had received the last of four intrathecal injections of methotrexate. Autopsy showed marked pulmonary edema as well as chronic lung changes, as previously described in patients with methotrexate pneumonitis. There is usually at least a 12-day interval from the onset of administration of methotrexate to the onset of the lung toxicity. The authors suggest the patient was sensitized by the intrathecal methotrexate and then reacted with angioneurotic edema of the lung when given the first oral dose of methotrexate. Careful examination for infectious agents, including electron microscopy, was negative.

Pitted keratolysis: a manifestation of human dermatophilosis.

A case of pitted keratolysis caused by Dermatophilus congolensis is reported. The organism was isolated from the lesion and identified by its morphological, cultural, and biochemical characteristics. A survey of the literature revealed that it rarely causes human infections, but is a common causative agent of disease in domesticated and wild animals. Human infections reported previously were traced to contact with infected animals or contaminated soil. We report pitted keratolysis in a 44-year-old physician with no known history of such a contact.

Manual sobre al fiebre amarilla y su diagnóstico diferencial histopatológico

A CONTINUACION SE REVISARA BREVEMENTE LA HISTORIANATURAL Y LAS CARACTE RISTICAS CLINICAS DE LA FIEBRE AMARILLA, PARA DESPUES HACER REFERENCIA A LA MORFOLOGIA MICROSCOPICA DE ESTA Y DE OTRAS ENFERMEDADES QUE EL PA TOLOGO PUEDE CONFUNDIR CON ELLA