Overview
Rickettsia rickettsii spotted fever is an acute endemic infectious disease caused by Rickettsia rickettsii transmitted by ticks, the disease is also known as Rocky Mountain spotted fever, tick-borne typhus. Clinical features include fever, headache and rash, and severe cases can be life-threatening. The population is generally susceptible, especially children and young people.
Causes
Rickettsia rickettsii is predominantly spherical and rod-shaped. After entering the body, the rickettsiae first bind to receptors on host cells and enter the host cells, and then multiply in local lymphatic tissues or intravascular epidermal tissues. It then spreads within the systemic vascular system via lymphatic fluid and blood, causing vascular inflammation and increased permeability, leading to massive cell breakdown and hemorrhage. In severe cases, the coagulation and kinin systems are activated, causing thrombotic obstruction, necrosis of the vascular musculature, and microembolization of the central nervous system, impairing the function of major organs such as the heart, lungs, kidneys, and central nervous system.
Some rickettsiae release phospholipase A, a phospholipid-solubilizing enzyme, upon invasion of the host, which can lead to cellular rupture when it accumulates in large numbers. Rickettsiae also release lipopolysaccharide, thus leading to endothelial cell damage and symptoms such as toxic shock.
Symptoms
1. Incubation period
Usually 2 to 14 days, with an average of 7 days. The larger the amount of Rickettsia rickettsii infection, the shorter the incubation period and the more serious the disease. After the incubation period, some patients may have a prodromal period of 1~3 days, which manifests symptoms such as loss of appetite, fatigue, weakness of limbs and chills.
2. Onset
Typical patients have a sudden onset of illness, with a sharp rise in body temperature to 39～40℃, and severe patients may have a super-high fever of 41℃ or above. There are chills, severe headache, generalized muscle and joint pain, photophobia and retro-ocular pain. Liver and spleen may appear enlarged. Without treatment of the pathogen, the fever does not subside, and the duration of the fever can be up to 2 to 3 weeks, after which the fever slowly subsides in most patients. In severe cases, Rickettsia rickettsii may aggravate damage to the vascular endothelium, resulting in thrombosis and local ischemic gangrene, which tends to occur in the skin at the tip of the nose, the earlobes, the scrotal area, and the fingers and toes. Limb necrosis and hemiparesis may occur if thrombosis of the aorta occurs. Severe patients often die from myocarditis and pulmonary edema.
(1) Rash 80% to 90% of patients in 3 ~ 4 days after the fever appeared pink rash, diameter of 2 ~ 5mm, began to be located in the wrists and ankles, and later extended to the arms, feet, chest, abdomen and maxillofacial. Two to three days after the appearance of the rash, the rash appears to melt and change to red or purple color.
(2) Petechiae During the recovery period, the rash gradually subsides and becomes petechiae on the palms of the hands, soles of the feet, ankles, and folds in the armpits, forming the characteristic distribution of the Rickettsia rickettsii fever rash. There may be transient hyperpigmentation and furfuraceous peeling after the rash subsides.
Examination
1. Laboratory tests
(1) Coagulation mechanism examination Severe patients may have decreased fibrinogen, prolonged prothrombin time and partial thromboplastin time, and even disseminated intravascular coagulation, leading to circulatory and other visceral dysfunction.
(2) Routine blood tests The peripheral white blood cell count decreases in the early stage, and is mostly in the normal range later on (the ratio of red blood cells to white blood cells in normal human peripheral blood is 6,000 to 1,000:1). It may be elevated in the case of severe or secondary bacterial infections. Secondary anemia may occur in the later stages of the disease.
(3) Cerebrospinal fluid examination In patients with neurologic disease, cerebrospinal fluid examination reveals elevated pressure and a mild increase in monocyte count and protein level.
(4) Immunological examination There are 3 methods: ① External Fibrinogen reaction OX19 and OX2 may show coagulation reaction, and the coagulation potency of OX19 and OX2 may increase 4-fold after a 2-week interval of reexamination, while OXk does not show positivity. Indirect immunofluorescence Antibody test and complement binding test may also show positive reactions, with a 4-fold increase in potency after 2 to 3 weeks. (iii) Skin and rash biopsies can detect Rickettsia rickettsii by immunofluorescence antibody test, which takes only 4 to 6 hours, and positive results can be obtained within 3 to 4 days of the disease, which is of significance for early and rapid diagnosis.
(5) Pathogenic examination: Rabbits or mice can be used to isolate the pathogen, and if positive results are found, the diagnosis will be confirmed.
2. Other auxiliary examinations
Abdominal ultrasound examination of the liver and spleen.
Diagnosis
A visit to an area where tick vectors are present within 2 weeks, a history of contact with animals carrying hard ticks or a history of hard tick bites are all useful references for epidemiology. Patients with acute fever, severe headache, photophobia, retrobulbar pain, and a pink rash on the wrists and ankles should be highly suspicious for the disease. Positive exo-Fibre reaction and immunologic findings favor the clinical diagnosis. Positive skin and rash biopsies with specific immunofluorescent antibodies and positive isolation of animal pathogens are diagnostic.
Differential diagnosis
1. The main differential diagnosis of this disease is measles, which can be differentiated with the help of the characteristics of measles oral mucosal Cortez spots.
Koplik’s spots appear on the oral mucosa, followed by maculopapular rash on the skin. At this point the measles virus proliferates in the invading cells, destroying them and causing inflammation.
2. Patients with central nervous system symptoms should be distinguished from the septicemic type of epidemic cerebrospinal meningitis, which can be identified with the help of the early appearance of petechiae and bruises in the septicemic type of epidemic cerebrospinal meningitis and the suppurative changes in the cerebrospinal fluid.
Epidemic cerebrospinal meningitis, referred to as meningitis, is a purulent meningitis caused by meningococcus. Clinical manifestations include fever, headache, vomiting, skin and mucous membrane petechiae, bruises and signs of meningeal irritation such as cervical rigidity.
Complications
Multiple complications of Rickettsia rickettsii spotted fever, such as shock, cardiac and renal failure, result in impaired function and can cause neurologic, respiratory, and circulatory complications. Some patients recover from the disease with sequelae such as deafness, loss of vision, inability to carry out work properly in the limbs, paralysis and recurrent episodes of erythema herpetiformis.
Treatment
1. Antibacterial drug treatment that affects the synthesis of bacterial proteins, the usage and dosage are as follows:
(1) Tetracycline orally and intravenously.
(2) Doxycycline orally.
(3) Chloramphenicol orally and intravenously.
The general patient pathogen treatment 2 to 3 days body temperature drop, antibacterial drugs course for 6 days. Quinolone antibacterial drugs are also effective. Due to the lack of cell wall of rickettsiae, penicillin and cephalosporin antibacterial drugs are ineffective.
2.Supportive therapy
Heavy patients provide enough nutrition and calories, maintain water, electrolyte and acid-base balance, and protect the function of important organs.
3. Glucocorticosteroids can be used in appropriate amount when the symptoms of poisoning are obvious or the headache is severe, its usage and dosage:
(1) High-dose surprise therapy for acute diseases. Such as severe infection and shock.
(2) General dose long-term therapy for autoimmune and allergic diseases.
(3) Small-dose replacement therapy.
(4) Alternate day therapy.
Prognosis
Rickettsial spotted fever is a serious infectious disease with a case fatality rate of 20% to 30%. The use of prompt and effective antimicrobials can reduce the case fatality rate to 3%. Patients with fulminant disease have irreversible progressive pathologic changes and can die within 3 to 5 days. The occurrence of severe cases has been associated with factors including advanced age at illness, untimely use of effective antimicrobials, and glucose-6-phosphate dehydrogenase deficiency in patients.