Microbial Diseases Service Investigators


Microbial Diseases Service Investigators

McCoy described the Microbial Diseases in 1911 while studying a plaguelike illness in ground squirrels in Tulare County, California. The first clinical description and bacteriologic proof of illness are attributed to Wherry and Lamb in 1914. In a series of studies conducted in Utah and elsewhere, Francis (1928) incriminated rabbits as important animal hosts and established the transmissibility of disease by deer flies. Etiology, Specific Laboratory Diagnosis, and Epidemiology.

Tularemia is of considerable increst because the causative micro-organism is a member of the important gram-negative group characterized by intracellular parasitism about which basic information on immunity mechanisms is incomplete. The bacillus is pleomorphic and non-motile and propagates best on such artificial media as blood glucose cysteine agar or following inoculation of animals with suspensions of infected tissues. Culture. During the early stages of illness, F. tularensis is isolated readily by direct culture inappropriate media or by the subcutaneous or intraperitoneal inoculation of exudate into mice or guinea pigs.

Positive cultures are obtained from the local ulcer or regional lymph nodes during the first several weeks in patients with a type of illness. Regardless of the clinical type of tularemia, viable organisms may be isolated from nasopharyngeal or gastric washings during the active. systemic phases of illness. Organisms have been. Impression smears of splenic tissues often reveal the characteristic coccal or bacillary forms intracellularly following preparation with Giemsa or Wayson's plague stain. Serologic Diagnosis. Maxi-mal titers are reached in about four weeks. Demonstration of a rise in titer through an examination of serial specimens is confirmatory evidence of infection, although single titers of 1:160 or more are usually significant.

Cutaneous Test Microbial Diseases

The reaction is of the delayed tuberculin-type, becoming positive in 48 hours. The test is highly specific and becomes positive during the first week of tularemia either prior to or coincident with the development of agglutinins. The test remains positive for years.

Epidemiology. Tularemia has been detected in many countries of the Northern Hemisphere. F. In much of North America, cottontail rabbits are the most important animal host and were formerly a very common source of the ulcers-glandular and typhoidal forms of tularemia. The restricted sale of wild rabbits in metropolitan areas resulted in a sharp decline of the disease. The clinical infection develops following puncture wounds by bony spicules of infected rabbits or by the ingestion of improperly cooked food. Streams are contaminated for variable periods by infected animal carcasses (or by other less well-understood routes), so that drinking the water or handling aquatic mammals such as muskrats may be hazardous.

In North America, the ticks Dermacentor ander, soni, Dermacentor variabilis, and the Lone Star tick are important reservoirs and vectors. Infected female ticks transmit F. tularensis transovarially. Tularemia occurs in all seasons: among hunters and trappers in the fall and winter, and during the spring and summer when ticks and deer flies are active. All ages and both sexes are susceptible. Mechanism of Infection and Pathology. The dis-ease may present in a variety of forms with two major subdivisions, depending on whether or not the initial site of entry can be visualized. In most instances, there is a primary ulcer, variable in size, which may be located on the skin (ulcers-glandular), in the eye, or in the nasopharynx with necrotizing lesions.

Sometimes the cutaneous lesion may be insignificant so that the picture is that of “glandular ‘tularemia” with-out an overt primary lesion. The entry also maybe through the intestinal tract (enteric or typhoidal) or via the lungs (pulmonary). Following infection, F. tularensis reaches the blood via the lymphatics and nodes; the microbe, although phagocytized, resides intracellularly without loss of viability. Granulomatous lesions develop within the reticuloendothelial system, particularly in lymph nodes, liver, and, spleen. These lesions, usually hyperplastic, bear some resemblance to tuberculosis and may caseate or form small local abscesses. The macrophage is the predominant cell type that surrounds an area of caseous necrosis. Bronchopneumonia is a common development in tularemia, occurring in approximately 30 percent of patients who acquire the disease, regardless of the type of infection.

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