Showing papers by "Gregory M. Anstead published in 2020"

History, Rats, Fleas, and Opossums: The Ascendency of Flea-Borne Typhus in the United States, 1910-1944

Abstract: Flea-borne typhus, due to Rickettsia typhi and Rickettsia felis, is an infection causing fever, headache, rash, hepatitis, thrombocytopenia, and diverse organ manifestations. Although most cases are self-limited, 26%–28% have complications and up to one-third require intensive care. Flea-borne typhus was recognized as an illness similar to epidemic typhus, but having a milder course, in the Southeastern United States and TX from 1913 into the 1920s. Kenneth Maxcy of the US Public Health Service (USPHS) first described the illness in detail and proposed a rodent reservoir and an arthropod vector. Other investigators of the USPHS (Eugene Dyer, Adolph Rumreich, Lucius Badger, Elmer Ceder, William Workman, and George Brigham) determined that the brown and black rats were reservoirs and various species of fleas, especially the Oriental rat flea, were the vectors. The disease was recognized as a health concern in the Southern United States in the 1920s and an increasing number of cases were observed in the 1930s and 1940s, with about 42,000 cases reported between 1931–1946. Attempts to control the disease in the 1930s by fumigation and rat proofing and extermination were unsuccessful. The dramatic increase in the number of cases from 1930 through 1944 was due to: the diversification of Southern agriculture away from cotton; the displacement of the smaller black rat by the larger brown rat in many areas; poor housing conditions during the Great Depression and World War II; and shortages of effective rodenticides and insecticides during World War II.

History, Rats, Fleas, and Opossums. II. The Decline and Resurgence of Flea-Borne Typhus in the United States, 1945-2019.

Abstract: Flea-borne typhus, due to Rickettsia typhi and R. felis, is an infection causing fever, headache, rash, and diverse organ manifestations that can result in critical illness or death. This is the second part of a two-part series describing the rise, decline, and resurgence of flea-borne typhus (FBT) in the United States over the last century. These studies illustrate the influence of historical events, social conditions, technology, and public health interventions on the prevalence of a vector-borne disease. Flea-borne typhus was an emerging disease, primarily in the Southern USA and California, from 1910 to 1945. The primary reservoirs in this period were the rats Rattus norvegicus and Ra. rattus and the main vector was the Oriental rat flea (Xenopsylla cheopis). The period 1930 to 1945 saw a dramatic rise in the number of reported cases. This was due to conditions favorable to the proliferation of rodents and their fleas during the Depression and World War II years, including: dilapidated, overcrowded housing; poor environmental sanitation; and the difficulty of importing insecticides and rodenticides during wartime. About 42,000 cases were reported between 1931-1946, and the actual number of cases may have been three-fold higher. The number of annual cases of FBT peaked in 1944 at 5401 cases. American involvement in World War II, in the short term, further perpetuated the epidemic of FBT by the increased production of food crops in the American South and by promoting crowded and unsanitary conditions in the Southern cities. However, ultimately, World War II proved to be a powerful catalyst in the control of FBT by improving standards of living and providing the tools for typhus control, such as synthetic insecticides and novel rodenticides. A vigorous program for the control of FBT was conducted by the US Public Health Service from 1945 to 1952, using insecticides, rodenticides, and environmental sanitation and remediation. Government programs and relative economic prosperity in the South also resulted in slum clearance and improved housing, which reduced rodent harborage. By 1956, the number of cases of FBT in the United States had dropped dramatically to only 98. Federally funded projects for rat control continued until the mid-1980s. Effective antibiotics for FBT, such as the tetracyclines, came into clinical practice in the late 1940s. The first diagnostic test for FBT, the Weil-Felix test, was found to have inadequate sensitivity and specificity and was replaced by complement fixation in the 1940s and the indirect fluorescent antibody test in the 1980s. A second organism causing FBT, R. felis, was discovered in 1990. Flea-borne typhus persists in the United States, primarily in South and Central Texas, the Los Angeles area, and Hawaii. In the former two areas, the opossum (Didelphis virginiana) and cats have replaced rats as the primary reservoirs, with the cat flea (Ctenocephalides felis) now as the most important vector. In Hawaii, 73% of cases occur in Maui County because it has lower rainfall than other areas. Despite great successes against FBT in the post-World War II era, it has proved difficult to eliminate because it is now associated with our companion animals, stray pets, opossums, and the cat flea, an abundant and non-selective vector. In the new millennium, cases of FBT are increasing in Texas and California. In 2018-2019, Los Angeles County experienced a resurgence of FBT, with rats as the reservoir.

Parinaud's Oculoglandular Syndrome: A Case in an Adult with Flea-Borne Typhus and a Review.

Abstract: Parinaud’s oculoglandular syndrome (POGS) is defined as unilateral granulomatous conjunctivitis and facial lymphadenopathy. The aims of the current study are to describe a case of POGS with uveitis due to flea-borne typhus (FBT) and to present a diagnostic and therapeutic approach to POGS. The patient, a 38-year old man, presented with persistent unilateral eye pain, fever, rash, preauricular and submandibular lymphadenopathy, and laboratory findings of FBT: hyponatremia, elevated transaminase and lactate dehydrogenase levels, thrombocytopenia, and hypoalbuminemia. His condition rapidly improved after starting doxycycline. Soon after hospitalization, he was diagnosed with uveitis, which responded to topical prednisolone. To derive a diagnostic and empiric therapeutic approach to POGS, we reviewed the cases of POGS from its various causes since 1976 to discern epidemiologic clues and determine successful diagnostic techniques and therapies; we found multiple cases due to cat scratch disease (CSD; due to Bartonella henselae) (twelve), tularemia (ten), sporotrichosis (three), Rickettsia conorii (three), R. typhi/felis (two), and herpes simplex virus (two) and single cases due to tuberculosis, paracoccidioidomycosis, Yersinia enterocolitica, Pasteurella multocida, Chlamydia trachomatis, Epstein–Barr virus, and Nocardia brasiliensis. Preauricular lymphadenopathy is a common clinical clue for POGS and is unusual in viral and bacterial conjunctivitis. For POGS, the major etiological consideration is B. henselae, which is usually diagnosed by the indirect immunofluorescence serologic technique. Although CSD POGS is usually self-limited, oral azithromycin may hasten resolution. However, other possible etiologies of POGS may also arise from cat or cat flea contact: sporotrichosis, tularemia, Pasteurella multocida, or FBT. If there is no cat contact, other epidemiologic and clinical findings should be sought, because several of these conditions, such as tularemia, paracoccidioidomycosis, and tuberculosis, may have grave systemic complications. Although there are usually no long-term ocular sequelae if POGS is properly diagnosed, it still may cause prolonged ocular discomfort and require multiple physician contacts.