Key knowledge points of infectious diseases
One. Manifestations of the infectious process :
1. Elimination of pathogens: non-specific immunity and specific immunity
2. Covert infection: Also known as subclinical infection. Refers to the pathogen invaded the human body, only induce the body to produce a specific immune response, without causing or only causing minor tissue damage, so that clinically do not show any symptoms, signs, or even biochemical changes, can only be found through immunological examination. Most pathogen infections are predominantly latent infections. Outcomes: Most were specifically immunized and the pathogen was removed; a minority became asymptomatic carriers, with the pathogen persisting in the body.
3. Overt infection: Also known as clinical infection. Refers to the pathogen invading the human body, not only induces the body to have an immune response, but also through the pathogen itself or the body's allergic reaction, resulting in tissue damage, causing pathological changes and clinical manifestations. Outcomes: The pathogen is removed and the infected person gains a relatively stable immunity; the immunity is not strong, and then the infection becomes the disease; and a small number become chronic pathogen carriers.
4. Carrier state: Carrying pathogen without obvious clinical symptoms.
According to the type of pathogen: those with viruses, bacteria, insects
Divided into episodes and durations: incubation period carriers, convalescent carriers, chronic carriers
Classification by duration of carrying: acute carriers (<3months), chronic carriers (>3months)
5. Latent infection (latent infection) pathogens infected with the human body after parasitizing in some parts, because the body's immune function is enough to localize the pathogen without causing overt infection, but not enough to remove the pathogen, the pathogen can be long-term latent, waiting for the body's immune function to decline, it can cause dominant infection. During this period, the pathogen is generally not excreted (it is not the source of infection, unlike the pathogen-carrying state).
Note: 1 ) Latent infection is the most common, followed by pathogenic carrying status, and the proportion of overt infection is the lowest
2) The above five forms of expression can be transformed into each other under certain conditions.
Two. Basic conditions of the epidemic process :
1. Source of infection: Refers to people and animals whose pathogens have grown, multiplied, and can be excreted from the body.
(1) Patients (2) Latent infected persons (3) Pathogen carriers (4) Infected animals
2. Route of transmission: The path by which a pathogen leaves the source of infection to reach another susceptible person.
(1) Respiratory transmission (2) Digestive tract transmission (3) Contact transmission (4) Insect vector transmission (5) Blood and body fluid transmission
3. Population susceptibility: People who lack specific immunity to an infectious disease are called susceptible persons, and they are susceptibility to pathogens. When the proportion of susceptible people in a particular population reaches a certain level, if there is a source of infection and a suitable route of transmission, it is easy to have an epidemic of the infectious disease.
Periodicity of infectious diseases: Some infectious diseases with strong post-morbid immunity will not occur until another epidemic occurs after an epidemic and when the proportion of susceptible people rises to a certain level again.
Three. Treatment of infectious diseases
(1) Treatment principle: Adhere to the principle of comprehensive treatment, that is, the principle of equal emphasis on treatment, nursing, isolation and disinfection, general treatment, symptomatic treatment and pathogenic treatment
( ii). Treatment: 1. General and supportive care 2. Pathogenic therapy 3. Symptomatic treatment 4. Rehabilitation 5. Traditional Chinese Medicine Treatment
Four. What are the types of notifiable infectious diseases in China? According to the prevention of Class A infectious diseases, what are the types of management?
There are 38 types of notifiable infectious diseases in 3 categories (2 in Class A, 25 in Class B, and 11 in Class C).
Category A (1. plague, 2. cholera) compulsory management of infectious diseases, urban requirements within 2 hours after detection, rural no more than 6 hours to report.
Category B (3. Infectious ATYPNUM , 4. AIDS, 5. Viral hepatitis, 6. Poliomyelitis, 7. Human infection with highly pathogenic avian influenza , 8. Measles, 9. Epidemic hemorrhagic fever, 10. Rabies, 11. Japanese encephalitis, 12. Dengue fever, 13. Anthrax, 14. Bacterial and amoebic dysentery, 15. Tuberculosis, 16. Typhoid and paratyphalitis, 17. Epidemic meningoccal meningitis, 18. Whooping cough, 19. Diphtheria, 20. Neonatal tetanus, 21. Scarlet fever, 22. Brucellosis, 23. Gonorrhea, 24. Syphilis, 25. Leptospirosis, 26. Schistosomiasis, 27. Malaria) for the strict management of infectious diseases, cities and towns require that within 6 hours after detection, rural areas do not exceed 12 hours to report, of which, for class B infectious diseases in infectious atypical pneumonia, anthrax in the lungs of anthrax and human infection with highly pathogenic avian influenza, take measures to prevent and control Class A infectious diseases.
Class C (28. influenza, 29. mumps, 30. rubella, 31. acute hemorrhagic conjunctivitis, 32. leprosy, 33. epidemic and endemic typhus, 34. kala-azar, 35. echinococcosis, 36. filariasis, 37. Infectious diarrhea diseases other than cholera, bacterial and amoebic dysentery, typhoid and paratyphoid 38. Hand-foot-and-mouth disease) are used to monitor and administer infectious diseases.
Five. Viral hepatitis is a group of infectious diseases with predominantly liver damage caused by a variety of hepatitis viruses. According to the etiological classification, there are currently hepatitis A, B, C, D and E. The clinical manifestations of various viral hepatitis are similar, mainly fatigue, loss of appetite, anorexia, and hepatomegaly, and some cases may have jaundice. Type A and E are transmitted by the fecal-oral route, which is manifested as acute hepatitis; type B, C, and D are mainly transmitted by the parenteral route, and most patients are chronically infected and can develop cirrhosis and hepatocellular carcinoma.
DNA virus: HBV deficiency virus: HDV Big Sanyang: HBsAg, HBcAb, HBeAg Small Sanyang: HBsAg, HBcAb, HBeAb Hepatitis A Prophylaxis: Hepatitis A vaccine, immunoglobulin Hepatitis E: Immunoglobulins have no preventive effect. Only acute hepatitis is caused by: Hepatitis A, Hepatitis E Fecal-oral transmission: Hepatitis A, Hepatitis E (HAV): No envelope, genome is a single strand of RNA. HBV: Contains cyclic double-strand DNA, HBsAg, DNA polymerase, core protein. HCV: The genome is a single strand of positive stranded RNA. HDV: The genome is a single strand of negative-stranded RNA. HEV: No envelope, genome is a single strand of positive-strand RNA )
★ Clinical manifestations of chronic hepatitis B, hepatitis C
Viral hepatitis B: The incubation period is 6 weeks to 6 months, usually around 3 months. Clinical manifestations include systemic symptoms, gastrointestinal symptoms, jaundice, pain in the hepatic region, hepatosplenomegaly, extrahepatic manifestations (liver disease face), and liver fibrosis.
Chronic hepatitis C: Mild symptoms manifested by common symptoms of hepatitis, such as easy fatigue, poor appetite, bloating, etc. It is also possible to be free of any conscious symptoms. Assay ALT fluctuated repeatedly, and HCVRNA remained positive. Liver function has been normal in 1/3 of patients with chronic HCV infection, persistent positive anti-HCV and HCVRNA, and liver biopsy may show chronic hepatitis and even cirrhosis.
Treatment of chronic liver disease: 1, general treatment 2, drug therapy: improvement and restoration of liver function, immunomodulation, anti-hepatic fibrosis, antiviral therapy (interferon preferred)
Clinical classification of viral hepatitis: According to clinical manifestations, it is divided into acute hepatitis (acute jaundice type, acute jaundice type), chronic hepatitis (mild, moderate and severe), severe hepatitis (acute, subacute, slow plus acute, chronic), cholestatic hepatitis, hepatitis cirrhosis.
Etiological diagnosis of hepatitis B: serum HBsAg, HBeAg, HBcAg, HBV-DNA, anti-HBC IgM, liver tissue HBeAg and/or HBsAg or HBV-DNA positive, can be diagnosed as current HBV infection, whether it is hepatitis B or what clinical type of hepatitis B depends on clinical symptoms, signs, liver function, liver histology tests.
Etiological diagnosis of hepatitis C: Hepatitis C can be diagnosed with both acute and chronic hepatitis clinical manifestations and a positive anti-HCV-IgM, anti-HCV-IgG, or HCV RNA positive.
★ The main clinical manifestations of severe hepatitis are described.
(1) Rapid deepening of jaundice, serum bilirubin higher than 171 μ mol/L ;(2) liver progressive shrinkage, liver odor; (3) bleeding tendency, PTA less than 40% ;(4) ascites, toxic drum intestine; (5) psychosyrheological symptoms (hepatic encephalopathy): timing, disorientation, decreased computing ability, mental abnormalities, restlessness, drowsiness, etc. Early hepatic coma can cause fluttering tremor; (6) hepatorenal syndrome: oliguria or even anuria, elevated blood urea nitrogen, etc.
6． Influenza: Acute respiratory infectious diseases caused by influenza virus, RNA virus, no cross-immunity. It is mainly manifested by sudden onset of illness, which can show symptoms of poisoning such as high fever, obvious headache, fatigue, and muscle aches throughout the body, and mild respiratory symptoms. There are three influenza viruses that can infect humans, influenza A is highly variable and often causes influenza pandemics, followed by influenza B, and influenza C virus antigenicity is very stable. The main sources of infection are influenza patients and latent infections. The route of transmission is mainly transmitted directly from person to person through droplets, but can also be transmitted indirectly through contact with contaminated hands, daily utensils, etc.
There are two important glycoproteins in the influenza virus envelope: hemoglutinin (HA) and neuraminidase (NA). Hemagglutinins can cause red blood cell agglutination and play an important role in the virus's entry into host cells. Neuraminidase assists in the release of viral particles and promotes their adhesion to respiratory epithelial cells and promotes the spread of viral particles.
Human avian influenza : an acute respiratory infectious disease caused by certain strains of influenza A virus infecting some strains in the avian subtype. The main clinical manifestations are hyperthermia cough and dyspnea, which may be accompanied by runny nose, nasal congestion, cough, sore throat, headache, muscle aches, and general malaise, followed by shortness of breath and significant manifestations of pneumonia. Route of transmission: respiratory transmission, through close contact with infected poultry and their secretions and excrements.
Highly pathogenic avian influenza: A class of acute respiratory infectious diseases that predominantly transmits from the respiratory tract caused by the H5N1 subtype. The main clinical manifestations are respiratory distress, lung consolidation, respiratory failure, and can also have complications such as toxemia, septic shock, renal failure, multi-organ failure and other complications and death.
7． Measles : Is an acute respiratory infectious disease caused by the measles virus, clinically characterized by fever, cough, runny nose, ocular binding memenitis, special oral measles mucosal spots [koplik's spots] and skin maculopapular rash.
Source of infection: man-made sole host of measles virus, acute patients as the most important source of infection (prodromal infection is the strongest) Transmission route: trans respiratory droplets
Eruption phase (extreme phase): fever on days 3 to 4 of the course.
a Fever and respiratory symptoms peak and symptoms of toxic blood worsen.
b Order of eruptions (top to bottom): behind the ear hairline – forehead, neck – thoracic and ventral back, limbs --- palms and soles of feet.
c Rash features: reddish maculopapular rash, pressure fading, normal skin between the rashes.
Eight. Renal syndrome hemorrhagic fever (HFRS) is a naturally occurring disease caused by hantavirus, with rats as the main source of infection. The main pathological changes are extensive damage to small blood vessels throughout the body, and the main clinical manifestations are fever, shock, congestion, bleeding and acute renal failure. The course of typical cases is five-stage.
Clinical manifestations: Incubation period 4-46d (7-14d)
Clinical features: fever, symptoms of systemic intoxication, bleeding Fever Hemorrhage Renal damage Renal damage In severe patients with severe patients with renal damage, fever is characterized by worsening of the disease.
1. Fever Phases during fever
(1) Fever Relaxing fever and retaining heat
(2) Symptoms of systemic poisoning Infectious-toxic Symptom Three pains: headache, low back pain, orbital pain.
Capillary Damage Three Reds: Red Face, Red Neck, Red Chest. Three swellings: bulbous conjunctiva, eyelids, facial swelling.
(4) Hemorrhage
(5) Renal damage
2. Hypotension shock phases
Hypotension Hypotension
Shock Hypotension hypotension tropesis Shock
Refractory shock refractory shock
3. Oliguric Phases in the oligulic phase
(1) Grading of oliguria : Oliguria: 24-hour urine output< 500 ml Anuria: 24-hour urine output < 50 ml
(2) Indexing of renal failure: mild moderate to severe
( 3 ) Types of renal failure: oliguria type Non-oliguria secondary renal failure Chronic renal failure
(4) Clinical manifestations of oliguria: Digestive tract symptoms Of the digestive tract symptom hypervolumia syndrome Hepervolumia Syndrome
Electrolyte, acid-base imbalance Hemorrhage
4. Polyuric Phases (1) Transitional period: 500-2000 ml (2) Early polyuria: > 2000 ml (3) Late polyuria: > 3000 ml Electrolytic disorders (low potassium and low sodium) and secondary infection and shock can occur.
5. Recovery Phases urine volume recovery below 2000 ml Blood urea nitrogen and hepatic anhydride are reduced to normal.
Nine. Epidemic Japanese encephalitis: it is an acute infectious disease with brain parenchymal damage caused by the Japanese encephalitis virus, transmitted by mosquitoes, and endemic in summer and autumn. It is mainly manifested by high fever, coma, convulsions, respiratory failure in severe cases, high mortality rate, and some sequelae.
Clinical manifestations: Incubation period: 4 to 21 days, average 10 to 14 days.
Typical performance of Japanese encephalitis:
1 ． Initial: days 1 to 3 of the course
At the beginning of the disease, it is manifested by acute fever, body temperature 39 to 40 °C, headache, nausea, vomiting, and drowsiness.
2 ． Extreme phase: days 4 to 10 of the course
( 1 ) High fever: body temperature above 40 °C, an average of 7 ~ 10 days, the longer the heat course, the more serious the disease.
( 2 ) Impaired consciousness: Varies from drowsiness to coma, usually 1 week, and the degree and duration of the disorder are related to the severity of the disease.
( 3 ) Convulsions or convulsions: the degree is different, can be from the local to the whole body, often accompanied by impaired consciousness, the cause of which is high fever, brain parenchymal damage and cerebral edema.
( 4 ) Respiratory failure: mainly central respiratory failure, is the main cause of death. Manifested by uneven respiratory rhythm and amplitude, herniation is associated with herniation, respiratory arrest in severe cases, and peripheral respiratory failure can be caused by respiratory muscle paralysis or sputum obstruction in a few cases. Hyperthermia, convulsions or convulsions, and respiratory failure are severe manifestations of the Japanese encephalitis extremum.
(5) Neurological signs and symptoms:
Shallow reflexes: weaken, disappear.
Deep reflexes: hyperactivity followed by disappearance. In coma, there may be limb ankylosing paralysis, hemiplegia, and high muscle tone.
Positive pyramidal bundle sign;
Positive for meningeal irritation;
Autonomic and cranial nerve damage;
(6) Circulatory failure: caused by cardiac insufficiency, cerebral edema and gastrointestinal bleeding.
3. Recovery period: within 6 months
After the extreme period, the body temperature decreases, the neuropsychiatric symptoms improve, about 2 weeks to recover, the heavy can have a variety of recovery period symptoms, low-grade fever, hyperhidrosis, aphasia, swallowing difficulty limb dysfunction, epilepsy, etc., half a year after the still unrecovered for the sequelae period.
4. Sequelae period:
5 to 20% of patients can have sequelae, mainly aphasia, impaired consciousness, limb paralysis and so on.
Clinical Type:
Type Body Temperature Consciousness Convulsions Meningeal Hypochondria Sequelae
Light 38~ 39 °C ( - ) ( - ) (±) ( -) —
Shallow coma in 39~ 40 °C Occasionally ( + ) (±) —
Weight 40 ° C coma repeatedly ( + ) ( + ) (±)
Critically ill above 40 ° C deep continuous ( + ) ( + ) ( + ) )
Ten. AIDS : Is an abbreviation for acquired immune deficiency syndrome (AIDS), a fatal chronic infectious disease caused by human immunodeficiency virus (HIV) infection. The disease is mainly transmitted through sexual contact and body fluids. It is characterized by HIV-specific violation of the central part of the human immune system - CD4+ T lymphocytes, so that the body's cellular immune function is seriously impaired, and finally complicated by various serious opportunistic infections and malignant tumors, leading to AIDS.
Route of transmission:
1. Sexual transmission: The leading cause of HIV transmission in the world.
2. Blood transmission :
(1) Intravenous drug use
(2) Blood transfusions and blood products
(3) Accidental exposure at the work of medical staff
(4) Iatrogenic transmission: acupuncture, surgery, endoscopy as potential transmission routes, organ transplantation, artificial insemination or contaminated instruments of HIV-infected people.
(5) Mosquito bites do not transmit AIDS. There is currently no evidence of transmission through food, water, insects or life contact.
3. Vertical mother-to-child transmission: If a pregnant woman is HIV positive, the probability of HIV infection in newborns is 11%-60%. include:
(1) The chance of placental transmission is 30%-40%.
(2) Transmission of childbirth There is a 50% chance of infection in newborns exposed to cervical and vaginal secretions.
(3) The probability of breastfeeding transmission is 10%-20%. HIV-positive pregnant women with low T4 lymphocyte count and high plasma viruses can increase the risk of transmission to newborns.
Eleven. Typhoid fever: is an acute intestinal infectious disease caused by Bacillus typhoid. Clinical features include persistent fever, apathy, symptoms of neurostoxicity and gastrointestinal tract, relative bradycardia, roseola, hepatosplenomegaly, and leukopenia. Sometimes serious complications such as intestinal bleeding (most common) and intestinal perforation (the most serious complication) can occur.
Route of transmission: Fecal-oral route. Water pollution is the main route and can cause outbreaks and epidemics.
Pathogenesis and pathological changes : After ingestion of Typhoid bacillus, the onset of the disease depends on the number and pathogenicity of Typhoid Bacillus and the immunity of the host. ( > 10 5 or more to cause the onset of the disease)
Typhoid cells Typhoid summary
Typhoid bacillus gastric bacteria are removed (normal gastric acid secretion, low number of bacteria)
The lower ileum invades the pooled lymph nodes to multiply and form the first lesion
(Transthoracic ductal intrusive mesenteric lymph nodes)
Blood circulation (first bacteremia)
Mononuclear-macrophage system engulfs reproduction
Blood circulation (second bacteremia) enters organs such as the hepatobiliary spleen
Excreted into the intestines and re-invaded the lymph nodes causing a more severe inflammatory response (ulcers, perforations)
bacteriological examination: blood culture and bone marrow culture are diagnostic methods.
(1) Blood culture: the positive rate is highest at weeks 1-2 of the course, gradually decreases after week 2, and is about 50% at the 3rd weekend.
(2) Bone marrow culture
(3) Stool culture: the positive rate increases gradually from week 2 of the course, and the positive rate is highest at weeks 3 to 4.
(4) Urine culture
In the fertilizer test, most patients were positive from week 2 of the course, positive at week 3 (50%), positive at weeks 4 to 5 (80%), and positive for several months after recovery.
When the O antibody titer is above 1:80 and the H antibody titer is above 1:160, or the O antibody titer is more than 4 times higher, it has auxiliary diagnostic significance.
Rekindling: When the clinical signs and symptoms of an infectious disease patient gradually decrease, but the body temperature has not yet fully returned to normal remission, the body temperature rises again due to the reproduction of pathogens lurking in the blood or tissues, and the symptoms and signs of the initial onset reappear.
Rekindling of typhoid fever: Some patients resurrect during the remission period, when the body temperature has not yet dropped to normal, and then rise again, and continue to recede after 5 to 7 days, which is called re-ignition.
Typhoid cells: Macrophages engulf typhoid bacilli, red blood cells, lymphocytes, and cell debris to form typhoid cells. Typhoid cells can form typhoid granulomas or typhoid nodules in clusters, which have pathological diagnostic value.
Relative bradycardia: refers to patients who are fever (especially hyperthermia), whose pulse acceleration is not proportional to the degree of increase in body temperature, and the patient's body temperature increases by less than 15 to 20 times per minute for each increase in body temperature, which is caused by increased parasympathetic excitability.
Black urinary fever: A large number of red blood cells parasitized by malaria parasites lyse in blood vessels, which can cause hyperhemoglobinemia, low back pain, soy sauce color urine, severe cases can appear moderate or more anemia, jaundice, and even acute renal failure, called hemolytic uremic syndrome, also known as black urine fever. This condition can also be induced by antimalarial drugs.
twelve. Bacterial food poisoning
Definition: An acute infectious toxic disease caused by eating food contaminated with bacteria or its toxins.
Clinical classification: gastrointestinal food poisoning, neurotic food poisoning
The main clinical features of gastrointestinal food poisoning: nausea, vomiting, abdominal pain, and diarrhea acute gastroenteritis are the main clinical manifestations.
Gastrointestinal food poisoning etiology: Salmonella, Vibrio parahaemolyticus, Escherichia coli, Proteus, Staphylococcus aureus, Bacillus cereus.
Neurotic food poisoning is defined as a toxic disease caused by eating food contaminated with Botox exotoxin. Botulinum toxin is a strictly anaerobic Clostridium Clostridium and is highly resistant.
13． Cholera: A fierce infectious disease caused by Vibrio cholerae, listed as a Class A infectious disease in China, sporadic in all seasons, epidemic in summer and autumn, mainly manifested as severe diarrhea and vomiting, resulting in a large amount of water, electrolyte loss (dehydration), acid-base imbalance, muscle spasm, severe peripheral circulation failure and kidney failure.
Route of transmission: water and food (faeces - mouth route)
Clinical manifestations of typical cholera:
1. Diarrhea and vomiting period: diarrhea first, vomiting after vomiting, no abdominal pain, no fever, no tenesmus after weight, stool from watery feces to rice swill water, vomit from gastric contents to rice swill, multi-ejection, can be accompanied by gastrocnemius muscle and rectus abdominal muscle spasm.
2. Dehydration period: ( 1 ) Dehydration manifestations: "cholera face", circulatory failure. ( 2 ) Electrolyte disorders: hypokalemia (3) metabolic acidosis
3. Reaction period: fever may occur due to toxin absorption after dehydration correction.
Treatment principles: (1) isolation according to intestinal infectious diseases (2) eating according to vomiting situation (3) intravenous or oral rehydration solution (4) symptomatic, antibiotic and inhibition of secretion
Rehydration: Fluid and electrolyte supplementation is a key part of the treatment of cholera, correcting dehydration, acidosis and electrolyte imbalances and improving cardiac function. The principle of rehydration should be early, rapid and sufficient, first salt after sugar, first fast and then slow, timely alkali supplementation, timely potassium supplementation. The total amount of liquid should include both positive dewatering and maintenance.
fourteen. Bacterial dysentery: an intestinal infectious disease caused by Shigella spp. (Dysentery bacillus), transmitted by the digestive tract; more common in summer and autumn in areas with poor sanitation. The main manifestations are abdominal pain, diarrhea, mucus, blood and pus with tenesmus, which may be accompanied by fever, and symptoms of systemic poisoning. In severe cases, septic shock and toxic encephalopathy appear.
★ Briefly describe the key points of differential diagnosis of toxic dysentery and Japanese encephalitis
(1) The onset of toxic dysentery is more acute than that of Japanese encephalitis, and high fever, convulsions and coma often occur within 24 hours of the onset of the disease, and the progression of Japanese encephalitis is relatively slow;
Toxic dysentery is often accompanied by circulatory failure (toxic shock), while Japanese encephalitis shock is rare, and impaired consciousness and meningeal irritation are obvious;
(3) Toxic dysentery generally has no meningeal irritation, and cerebrospinal fluid examination is mostly normal, while Japanese encephal fluid examination has abnormal changes (consistent with viral encephalitis changes);
swabs or saline enemas with toxic dysentery are shown on stool microscopy with most white blood cells and/or pus cells and red blood cells, while patients with Japanese encephalitis are positive for Japanese encephalitis-specific IgM antibodies.
fifteen. Meningitis epidemic: is an acute purulent meningitis transmitted by Neisseria meningitidis (Diplococcus meningitidis) through the respiratory tract, which is characterized by sudden high fever, severe headache, vomiting, petechial petechiae of the skin and mucosa, and meningeal irritation, and some sepsis shock and brain parenchymal damage. The disease is more common in winter and spring, and is more common in children.
sixteen. Sepsis: Refers to an acute systemic infection that occurs when pathogenic or conditional pathogenic bacteria invade the blood circulation and grow and multiply in the blood to produce toxins. If the bacteria that invade the bloodstream are cleared by the body's defenses, it is called bacteriemia when there are no obvious symptoms of toxicemia. Sepsis with multiple abscesses with a longer course of illness is called pyemia .
Bacteria that cause sepsis: there are gram-positive cocci, gram-negative bacilli, anaerobic bacteria, fungi, etc. Gram-positive cocci are predominantly staphylococcus, enterococcus, and streptococci, the most common being Staphylococcus aureus, especially methicillin-resistant Staphylococcus. Common gram-negative bacilli are Escherichia coli, Pseudomonas, Klebsiella, Proteus, and Acinetobacter.
Common manifestations of sepsis: symptoms of toxicity (chills, high fever), rash (petechiae), joint damage, hepatosplenomegaly, primary lesions, migratory lesions.
seventeen. Leptospirosis: An acute zoonotic infectious disease caused by the pathogenic leptospirosis. Rodents and pigs are the main source of infection, infected by contact with hook-containing infested water through skin and mucous membranes. There are distinctly popular, regional, seasonal (summer and autumn) and occupational (farmers, slaughterers, sewers, hunters, etc.). The main clinical manifestations are acute onset of hyperthermia, conjunctival hyperemia, superficial lymphadenopathy, and gastrocnemius tenderness.
【Clinical Manifestations】
( 1 ) Early (hook body sepsis phase):
Fever: acute onset of fever, accompanied by chills or chills, mostly residual heat, heat range of about 7 days.
Pain: Headache is pronounced, usually in the forehead. Muscle aches throughout the body, including the neck, chest, abdomen, back muscles, and leg muscles.
Fatigue: Fatigue is pronounced, especially in the legs, and even inability to stand and walk.
Conjunctival hyperemia: appears on the first day and worsens rapidly.
Gastrocnemius myalgia: it can appear on the first day of illness, there is mild tenderness, severe pain is severe, can not walk, refuse to press.
Superficial lymphadenopathy: inguinal lymph nodes are more common, followed by axillary lymph nodes, soft and tender.
Others: sore throat, hyperemia, enlarged tonsils, etc.
Summary: "Fever and soreness, lack of pain, red eyes and legs hurt and knots"
This phase lasts 3 to 5 days, at which point the hook body disappears from the blood and cerebrospinal fluid.
(2) Intermediate period (organ damage phase)
According to the main clinical characteristics, it can be divided into the following types: infection poisoning type (also known as influenza typhoid type), jaundice hemorrhagic type, pulmonary hemorrhage, renal failure type, meningoencephalitis type.
1) Infection poisoning type (also known as influenza typhoid type): the three symptoms are fever, systemic muscle aches and fatigue; the three signs are conjunctival hyperemia, gastrocnemius muscle tenderness and superficial lymphadenopathy and tenderness, which are common manifestations of other types of hook body disease in the early stage.
2) Pulmonary hemorrhage type: the disease worsens after 3 to 4 days, and there are different degrees of pulmonary hemorrhage, which are divided into mild pulmonary hemorrhage type and pulmonary diffuse hemorrhage type, the latter with a high case fatality rate. The latter can also be divided into aura (x-ray is a dot-like shadow or small-piece fusion), bleeding period (x-ray is a wide-scale punctate or large fusion of both lungs), and dying period (delirium, irregular breathing, massive hemoptysis).
3) Jaundice bleeding type: on the 4th to 8th day of illness, progressively aggravated jaundice, bleeding tendency and kidney damage, renal failure as the main causes of death.
Liver damage: loss of appetite, nausea, vomiting, elevated ALT, mild to moderate enlargement of the liver, tenderness, mild enlargement of the spleen.
Bleeding: frequent nosebleeds, ecchymosis of the mucous membranes of the skin, coughing up blood, blood in the urine, bleeding from the vagina, in severe cases, heavy bleeding of the digestive tract causing shock or death.
Renal damage: proteinuria, hematuria, casts, renal failure in severe cases.
4) Renal failure type: renal damage is very common in leptosomiasis, mainly manifested in proteinuria and a small number of cells and casts, only severe cases can appear azotemia, oliguria or anauria, this type often coexists with jaundice hemorrhagic type.
5) Meningoencephalitis type: meningitis or encephalitis appears in the course of the disease in 3 to 4 days, and the cerebrospinal fluid changes.
(3) Post-post-fever, post-ocular onset, reactive meningitis, cerebral arteritis obliterans
【Laboratory Tests】
General examination: the total number of blood white blood cells and neutrophils is mildly elevated or normal, 2/3 of patients have mild proteinuria in the urine routine, urine tests can show red blood cells, white blood cells and casts, and the number of platelets in severe patients is decreased.
Serological test Microcoagulation test MAT: check for the presence of specific antibodies in the serum, positive one week after the general disease, gradually increased, positive for the potency of more than 1:400, and positive for the potency increased by four times in the 2-week interval in the endemic area. A positive confirms the diagnosis.
【Diagnosis】 Diagnosis of hook body disease is based on: (1) epidemiological data: hook body disease water contact history, summer and autumn onset, local epidemic situation; (2) clinical manifestations: with the basic characteristics of hook body disease such as acute onset, fever and systemic poisoning symptoms, leg pain, gastrocnemius muscle and tenderness are obvious, superficial lymphadenopathy, conjunctival hyperemia. The jaundice hemorrhagic form has jaundice, bleeding, and renal impairment on the basis of the above clinical manifestations. The pulmonary hemorrhage type presents with pulmonary hemorrhage based on the basic features. The meningoencephalitis type has intracranial hypertension, meningeal irritation, and neuropsychiatric abnormalities. (3) Laboratory data: the number of WBCs increases, the ESR accelerates, the hook body coagulation test is positive > 1/400, or the titer of the early and convalescent double serum antibodies increases by more than 4 times, which can confirm the diagnosis. Hook-body DNA testing is useful for early diagnosis.
【Treatment】 Pathogen treatment: Killing pathogenic bacteria is the key and fundamental measure to treat this disease, emphasizing the early application of effective antibiotics. Such as penicillin (preferred), gentamicin, tetracycline.
Hatch reaction: After receiving the first dose of penicillin or other antibacterial drugs, patients with hook disease can be cracked due to the killing of a large number of hooks in a short period of time to explain the aggravation of clinical symptoms caused by the release of toxins, common high fever, chills, and decreased blood pressure, called Hersch's reaction. Treatment with sedation and intravenous infusion or hydrocortisone as soon as possible after occurrence.
18． Malaria: An infectious disease caused by parasitism of the malaria parasite in humans, it is mainly transmitted by the bite of female Anopheles mosquitoes. Infected by malaria vector bite or input into the blood of people with malaria parasites, malaria parasitism parasitizes in human liver cells or red blood cells, and proliferates in red blood cells, so that red blood cells rupture in batches and become ill, and the clinical manifestations are characterized by intermittent chills, high fever, sweating and fever reduction, and anemia, splenomegaly and so on can occur after multiple attacks. Relapse of vivax malaria and ovoid malaria, and there are no delayed sporospores and no recurrence of three-day malaria and falciparum malaria.
【Treatment】 Chloroquine and boanquine Chloroquine: drugs that kill the proliferation of the malaria parasite in the internal rift of red blood cells. Boanquine: drugs that kill the gametosomes and late-onset sporozoites of the plasmodium in red blood cells.
nineteen. Schistosomiasis: A parasitic disease caused by parasitizing the venous system in the human body and is infected by skin contact with the infected water of tail cercles. The acute phase is characterized by fever, hepatomegaly with tenderness, white blood cell count and significant increase in eosinophils and dysentery stools, and there may be significant hepatic fibrosis in the late stage, accompanied by portal hypertension such as macrolysis, ascites and other major manifestations.
In the life history of Japanese schistosomiasis, humans are the terminal host, snails are the only intermediate hosts required, in addition to humans, there are 41 kinds of mammals such as cattle, sheep, pigs, dogs, cats that can be used as its host for insects.
The route of transmission requires three conditions: feces into the water, the presence of snails, and host contact with the infected water. Schistosomiasis in Japan is a zoonotic disease, and the source of infection is the patient and the host of the carnivodia.
Concomitant immunity: Partial immunity can be obtained after human infection with schistosomiasis, and there are still adult parasites and laying eggs in the portal vein of the patient, but the host has a certain immunity to re-infection, without damaging the adults in the body, this immunity is called concomitant immunity.
twenty. Intestinal amoeba disease: Amoebic sacs contaminate food and water, and oral infection is the main route of transmission.
Pathological changes: lesions in the colon, in turn more common in the cecum, ascending colon, rectum, sigmoid colon, appendix and terminal of the ileum. Typical initial lesions are small, scattered superficial erosions, followed by the formation of more isolated and lighter-colored small abscesses, and after rupture, the formation of flask-like ulcers with irregular edges and large mouths, the basal layer of the mucous membrane, the cavity is filled with brownish yellow necrotic substances, containing lyzed cell fragments, mucus and trophozoites.
Complications: Intestinal complications: (1) Intestinal bleeding. (2) Intestinal perforation (the most severe). (3) Appendicitis. (4) Colon lesions. (5) Rectum - perianal fistula.
Identification points
Acute bacterial dysentery
Acute amoebic dysentery
pathogen
Shigella
Tissue-lysolytic amoeba trophozoites
epidemiology
Sporadic, endemic
Sporadic
latent period
Hours to 7 days
Weeks to months
Clinical manifestations
There are many symptoms of fever and poisonous blood, abdominal pain is severe, there is ten or dozens of times a day, diarrhea is more than ten or dozens of times a day, mostly left lower quadrant tenderness
More fever, less toxic blood symptoms, mild abdominal pain, no tenoli, diarrhea several times a day, mostly tenderness in the right lower quadrant
Stool examination
Stool volume is small, mucus pus and blood stool, microscopy has a large number of white blood cells and red blood cells, visible phagocytes, fecal culture has Shigella growth
High stool volume, dark red jam-like stool, strong smell, microscopic examination of leukocytes, more red blood cells, with Schalketone crystals, can find tissue-lysolytic amoeba trophozoites
Blood leukocytes
The total number and neutrophils are significantly increased
Slightly increased in the early days
Colonoscopy
Diffuse congestion, edema and superficial ulceration of the intestinal mucosa, lesions are mainly rectum and sigmoid colon
The intestinal mucosa is mostly normal, with deep ulcers scattered around it, a red halo around it, and lesions mainly in the cecum, ascending colon, followed by sigmoid colon and rectum