| disease | Xinjiang Hemorrhagic Fever |
| alias | Xinjiang Hemorrhagic Fever, XHF |
Xinjiang hemorrhagic fever (XHF) is a natural epidemic disease caused by a virus and transmitted by hard ticks. It is clinically characterized by fever, headache, hemorrhage, and hypotensive shock.
bubble_chart Epidemiology
The disease was first discovered in Crimea, Russia in 1944, and then in Congo, Africa in 1956. In 1965, it was first identified in the Bachu region of Xinjiang, China, with the banks of the Tarim River being the natural epidemic focus of the disease, more severe in the upstream areas. New natural epidemic foci frequently appear in both northern and southern Xinjiang. Besides Xinjiang, several cases of patients with positive antibodies for this disease were found in Yunnan in 1982. In 1988, positive antibodies were found in sheep serum in the semi-desert areas of Qinghai, and in 1991, positive antibodies for this disease were also detected in sheep serum in the grasslands of Sichuan, indicating that there are widespread natural epidemic foci of this disease in the northwest and southwest regions of China. The disease is prevalent in Crimea, the lower reaches of the Don River, the Volga River basin in Russia, and Africa, also known as Crimean hemorrhagic fever (CHF) or Crimean-Congo hemorrhagic fever (CCHF).
The main sources of the pestilence are sheep and Tarim hares in the epidemic areas. In addition, goats, cattle, horses, camels, hares, and foxes may also be sources of the pestilence. Patients in the acute phase are also sources of the pestilence. The Asian Hyalomma tick (Hyatomma asiaticum, a type of hard tick) is the main vector of the disease. The ticks mainly exist in the fallen leaves under the poplar trees and transmit the disease to humans and animals through bites. The virus can be passed on through tick eggs, so the Asian Hyalomma tick is also a reservoir host of the virus. In addition, contact with infected sheep blood or the blood of patients in the acute phase through skin wounds can infect humans, and ingestion of virus-contaminated food can also lead to infection.
The population is generally susceptible, but it is more common among young adults, and the onset of the disease is related to grazing. There is a latent infection in the population of the epidemic area, and neutralizing antibodies appear on the 6th day after the onset of the disease, reaching a peak in two weeks, and lasting immunity can be obtained after the disease.The epidemic season is from March to June, with a peak in April and May, showing a sporadic epidemic.
The pathogen of this disease is an arthropod-borne RNA virus, which is round or oval in shape, with an outer envelope, and has a diameter of 85-105 nm. It is classified under the Bunyaviridae family and the Nairovirus genus. This virus is the same as the Crimean-Congo hemorrhagic fever (CCHF) virus. It is pathogenic to newborn white mice, rats, and golden hamsters, and can propagate and cross-passage in the brains of suckling mice, chicken embryos, hamster kidneys, white mouse kidneys, suckling rabbit kidneys, and Vero-E6 cells. It is sensitive to lipid solvents, ether, chloroform, and sodium deoxycholate. It can be inactivated by exposure to a pH below 3.0 for 90 minutes or by heating at 56°C for 30 minutes. Low concentrations of formaldehyde can inactivate it while preserving its antigenicity. After vacuum drying, it can be stored at 4°C for several years.
bubble_chart Pathological Changes
The fundamental pathological changes of this disease involve systemic capillary dilation, congestion, increased permeability and fragility, leading to varying degrees of congestion and hemorrhage in the skin, mucous membranes, and tissues of various organs throughout the body. Substantive organs such as the liver, adrenal glands, and pituitary gland exhibit degeneration and necrosis, with gelatinous edema present behind the abdominal membrane.
The incubation period is 2 to 10 days. The onset is abrupt, with shivering, high fever, headache, lumbago, general body pain, thirst, vomiting, flushing of the skin on the face and chest, edema of the bulbar conjunctiva, hemorrhagic spots on the soft palate and buccal mucosa, petechiae and ecchymoses on the upper chest, armpits, and back, and epistaxis. The febrile course lasts about 1 week. Hypotensive shock and hemorrhagic phenomena, such as gastrointestinal bleeding, hematuria, and uterine bleeding, occur before and after the fever subsides. The disease course lasts about 10 to 14 days. There is no oliguric or polyuric phase.
bubble_chart Auxiliary Examination
The blood count shows a decrease in white blood cells and platelets, with an increase in lymphocytes and the presence of abnormal lymphocytes in the differential count. There is protein in the urine. The fecal occult blood test is mostly positive. Bleeding and clotting times are prolonged, and clot retraction is poor.
Virus isolation: Virus can be isolated from the blood of early-stage patients.
Serological tests include complement fixation test, neutralization test, reverse passive hemagglutination test, indirect immunofluorescence test, hemagglutination inhibition test, and double immunodiffusion test. A fourfold or greater increase in antibody titer in paired sera is diagnostically significant.
The diagnosis primarily relies on epidemiological data, including a history of effective herding or fieldwork in endemic areas and seasons, contact with sheep, rabbits, cattle, or patients in the acute phase, and a history of tick bites. Clinical manifestations include sudden onset, shivering, high fever, headache, lumbago, thirst, vomiting, hemorrhagic spots on mucous membranes and skin, and significant bleeding phenomena and/or hypotensive shock during the course of the disease. Laboratory tests show a decrease in both white blood cells and platelets, an increase in lymphocytes, and the presence of abnormal lymphocytes. A confirmed diagnosis can be made if the antibody titer in paired serum samples increases by more than four times in complement fixation tests and neutralization tests.
bubble_chart Treatment Measures
Based on the pathophysiological changes of the patient, a comprehensive therapy is adopted. Early diagnosis and early treatment can alleviate the progression of the disease. For early-stage patients with fever, intravenous infusion is administered to replenish sufficient fluids and electrolytes, and the application of adrenal corticosteroids has shown certain efficacy. In recent years, the use of freeze-dried therapeutic serum prepared from infected sheep serum has achieved good results in early treatment. Usage: For those with negative skin allergy tests, 10-15ml of therapeutic serum is administered via intramuscular injection once. Ribavirin, due to its significant inhibitory effect on the virus, may have certain efficacy in early treatment. For severe patients presenting with shock, cavity bleeding, pulmonary edema, etc., treatment can be referred to that of epidemic hemorrhagic fever.
The case fatality rate of this disease is high, generally around 25%. Patients with severe bleeding or shock have a poor prognosis.
Preventing and eliminating ticks are the main measures to prevent this disease. Lyme Stop has a certain repellent effect on ticks, while Shenzhou Crown, Radar Aerosol, and Weihaijing all have significant tick-killing effects. Isolate patients and ensure personal protection measures are in place.
