Brazilian Purple Fever
Introduction
Introduction to Brazilian Purple In 1984, he was first discovered in a pediatric acute fulminant infectious disease in São Paulo, Brazil. His clinical manifestations include high fever, abdominal pain, vomiting, purpuric rash, shock, etc., which can die very quickly. More than 90% of patients have had suppurative conjunctivitis about half a month before the disease. In 1985, a panel of experts from the Pan American Expert Group and the US CDC conducted research on pathogens, epidemiology, clinical manifestations, and laboratory tests, and considered a new disease named BPF. In 1986, Haemophilus influenzae biogroupaegyptius (HIBA) isolated from the blood, cerebrospinal fluid and purpura of typical patients was confirmed as its pathogen. basic knowledge The proportion of illness: 0.003% Susceptible people: no specific people Mode of infection: non-infectious complication:
Cause
Brazilian purple fever
(1) Causes of the disease
The bacteria were originally called Koch-Weeks bacillus. In 1950, Pittman et al. named Haemophilus hominis. In 1976, Killa reported that the phenotype of Haemophilus hominis was very similar to that of influenza B., which was named as Haemophilus influenzae. (Haemophilus influenzae biogroup aegyptius, HIBA), HIBA (called BPF strain) obtained from the blood or cerebrospinal fluid of a typical Brazilian purple fever patient, compared with HIBA (control strain) which only causes conjunctivitis, and found that the BPF strain contains a molecular weight of 0.024. The plasmid and the control strain contained a plasmid with a molecular weight of 0.002 or no plasmid; the whole bacterial component was electrophoresed, and the hybrid phase of 16 23S RNA of Escherichia coli was used as a probe, and the extracellular protein was studied, and the BPF strain and the control strain were found. There are obvious differences. Due to the above differences, HIBA bacteria have different pathogenic abilities and cause different clinical manifestations.
(two) pathogenesis
HIBA bacteria invade the eyes, and proliferate locally and cause inflammation after the nose and throat. The invasive BPF strain enters the bloodstream and causes bacteremia, releasing endotoxin. The average endotoxin in the blood of the child is 675g/L (675pg). /ml), the average value of healthy children is 25g / L (25pg / ml), so endotoxin may be an important cause of multiple organ damage, autopsy found skin, mucous membranes have extensive ecchymoses and purpura, small blood vessels of various tissues There may be microthrombus formation, hemorrhage and necrosis; brain edema but no inflammation; lung congestion, edema and hemorrhage; adrenal gland bleeding; lymphocytes in the spleen and lymph nodes are significantly reduced; some limbs distal and ear, nose There was ischemic necrosis at the same place, but no vasculitis was seen.
Prevention
Brazilian purple fever prevention
Curing conjunctivitis still can not prevent the occurrence of BPF, it is recommended to use ampicillin or chloramphenicol to drop the eyes, it should be used for a few days to prevent the occurrence of BPF, the epidemic situation should be monitored in the epidemic areas, to understand the BPF strain in the local The situation of growth and decline, predicting the possibility of BPF epidemic, and taking appropriate preventive measures.
Complication
Brazilian purple fever complications Complication
Concurrent DIC, acidosis, etc.
Symptom
Brazilian purple fever symptoms common symptoms blood pressure drop less urinary abdominal pain diarrhea unclear hair gastrointestinal bleeding hemorrhoids fever
1. Brazilian children with purple fever often suffer from suppurative conjunctivitis. After several days of conjunctivitis regression, the child suddenly has high fever, vomiting, abdominal pain, and may have diarrhea. After 12 to 24 hours of fever, the skin and mucous membranes appear purpura and quickly spread to the trunk. Limbs and face, accompanied by blood pressure drop, gastrointestinal bleeding, oliguria, cyanosis, etc., hand, foot, ear, nose can appear gangrene, can also be accompanied by DIC, acidosis, children with unconsciousness, more in 1 ~ Death within 2 days, the case fatality rate was 70%, some children with blood culture BPF strain positive, but no purpura and shock, the prognosis is good, may be related to bacterial virulence and early antibacterial treatment.
2. Suppurative conjunctivitis can be caused by a highly virulent BPF strain, or by non-BPF HIBA, and the clinical manifestations are no different from those of other bacteria-induced suppurative conjunctivitis.
Examine
Brazilian purple fever check
1. The peripheral blood leukocytes of blood can increase to about 15×109/L, and the rod-shaped and lobular granulocytes increase, and the platelets can be reduced.
2. The pathogen examination should be taken as soon as possible for bacterial culture. For example, HIBA can be cultured from blood, cerebrospinal fluid and purpura to diagnose BPF. However, if HIBA is obtained from eye secretion and nasopharyngeal culture, bacterial identification is required. Test to determine whether it is a BPF strain. It is known that BPF strains have a pilin protein antigen with a molecular weight of 25000. The specific antibody obtained by immunizing animals with this antigen can be distinguished from the cultured HIBA by immunoassay. Whether it is BPF strain, the established detection methods are;
1 enzyme immunoassay (EIA): the specific molecular weight of BPF strain detected by specific monoclonal IgM and IgG2b antibodies is 25×103,
2 slide agglutination test: detection of polyclonal antibodies against pili antigen, satisfactory sensitivity and specificity, because the experiment is simple, fast and cheap, Brazil has been used to predict whether BPF is popular,
3 latex agglutination test (LIA): a polyclonal antibody coated with latex particles as pilus protein, which is more sensitive than monoclonal antibody.
4 spot immunoassay: can directly detect whether there is a BPF strain with a molecular weight of 25×103 and pili on the secretion of the eye of patients with conjunctivitis, and the identification result can be obtained more quickly.
3. Other tests for liver and kidney function can be impaired, transaminase, urea nitrogen can be increased, prothrombin time can be extended for 36s (16 ~ 90s), blood oxygen content can be reduced, and DIC and metabolic acidosis can occur. Although there is no pathological change of meningitis, the cerebrospinal fluid examination of white blood cells can be slightly increased, with an average of 26 × 106 / L, multinuclear majority, sugar and chloride are in the normal range.
Liver and kidney function can be impaired, transaminase, urea nitrogen and the like can be elevated.
Diagnosis
Brazilian purple fever diagnosis
Currently known in Brazil, Australia and Australia, the United States can also report suspected cases, mostly in the warm season, localized purulent conjunctivitis epidemic, patients are children under 10 years of age, clinical features of acute high fever, abdominal pain, Vomiting, purulent skin mucosa appeared 1 to 2 days later, suffering from purulent conjunctivitis in the first half month before the disease, blood leukocytes can be increased, platelets can be reduced, and HIBA bacteria obtained from BPF strain in blood culture are the basis for diagnosis.
The disease was initially misdiagnosed as fulminant epidemic cerebrospinal meningitis, but there is no obvious inflammatory change in cerebrospinal fluid. The most important differential diagnosis is bacterial culture, which can be differentiated from bacteremia and sepsis caused by various bacterial infections.
