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Bacterial infectious diseases mind map
This is a mind map about bacterial infectious diseases, including brucellosis, meningococcal meningitis, typhoid fever, bacillary dysentery, etc. Hope this helps!
Edited at 2023-11-05 14:10:35
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
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Bacterial infectious diseases mind map
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
- Reproductive development of animals
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
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- Outline
bacterial infectious diseases
cholera
Cholera is a severe intestinal infectious disease caused by Vibrio cholerae, secretory diarrhea, and is a Class A infectious disease in my country. Typical clinical manifestations are: acute onset, severe diarrhea, often accompanied by vomiting, and resulting dehydration and muscle spasms. In severe cases, circulatory failure and acute renal failure may occur.
etiology
biological characteristics
Gram-negative arc-shaped or comma-shaped bacilli
The bacterial cells are active and move like shuttles under dark-field hanging drop microscopy. A direct smear of feces shows a "school of fish" appearance.
It is a facultative anaerobic bacterium that reproduces faster in an alkaline environment. It can be cultured using 1% alkaline peptone water with pH 8.4-8.6.
Pathogenicity
Flagellar motility, mucin-lytic enzymes, adhesins, toxin synergistic pili A, cholera enterotoxin
resistance
Sensitive to dryness, heat, acid, and general disinfectants
O139 survives longer than O1
Classification
Vibrio cholerae group O1 (main pathogenic bacteria)
Non-O1 Vibrio cholerae
Atypical O1 group Vibrio cholerae
Epidemiology
The world’s seven pandemics
Source of infection
patients and carriers
way for spreading
Water sources and food contaminated by Vibrio cholerae can cause outbreaks, and are indirectly transmitted through daily contact and flies.
Susceptible groups
Generally susceptible, mostly invisible infections
The epidemic season in my country is summer and autumn, July to October; there is no family gathering, and the disease is mainly in adults, with more males than females; the existing cholera vaccine has no protective effect against O₁₃₉
Pathogenesis and pathology
Pathogenesis
Immunity
Normal stomach acid can kill certain bacteria
The number of Vibrio invasions
Pathogenicity
Pathophysiology
water and electrolyte imbalance
Dehydration; the fluid lost is isotonic fluid, which contains a lot of potassium
Metabolic acidosis (acid-base imbalance)
Caused by loss of large amounts of bicarbonate. Circulatory failure→hypoxia→excessive production of lactic acid→aggravated acidosis; acute renal failure
pathology
severe dehydration
clinical manifestations
The incubation period is 1 to 3 days, no more than 5 days
installment
Diarrhea and vomiting period (a few hours or 1 to 2 days)
diarrhea
Painless severe diarrhea without tenesmus or fever
Yellow, rice-like, washed-meat-like
Vomit
Diarrhea first and then vomiting, no nausea, projectile vomiting
dehydration period
dehydration
Mild rehydration 3000~4000ml
Moderate 4000~8000ml
Heavy 8000~12000ml
muscle spasms
Low sodium causes gastrocnemius and rectus abdominis muscle spasms
Hypokalemia
Uremia, acidosis
Increased breathing and impaired consciousness
circulatory failure
Hypovolemic shock due to severe water loss
recovery period/reaction period
subtopic
dry cholera
Toxic cholera has an acute onset, without diarrhea or vomiting, and rapidly enters toxic shock and leads to death.
laboratory tests
Blood routine: hemoconcentration
Blood biochemical tests: serum potassium, sodium, and chloride are normal or decreased, and sodium bicarbonate decreases;
Urine routine: protein, RBC, casts;
Serological tests: antibacterial antibody and antiviral antibody tests
Molecular biology technology: PCR method can detect pathogenic bacteria
Stool culture (preferred)
complication
acute renal failure
Hypovolemic shock is not corrected in time
acute pulmonary edema
Metabolic acidosis leads to pulmonary hypertension and pulmonary edema
diagnosis
Diagnostic criteria
Diarrhea symptoms: Stool culture positive for Vibrio cholerae
During the cholera epidemic, typical symptoms appeared in the epidemic area. Although the stool culture was negative, the serological antibody titer increased by more than 4 times.
During the epidemiological investigation, it was found that there were diarrhea symptoms and contact history (mild cholera) within 5 days before and after the positive stool test.
Choose one
Suspected diagnosis criteria
First-time case with typical symptoms of cholera, but the etiology is unknown
There was a clear history of contact during the epidemic, and there were symptoms of vomiting and diarrhea, but there was no other explanation.
Deny the suspected diagnosis
3 stool cultures and 2 serologies were negative
identify
Training is the gold standard
treat
Strict isolation
, strictly isolate and report in a timely manner according to Class A infectious diseases
Timely rehydration
Early, fast and sufficient
Salt first and then sugar, first fast and then slow
Acid correction and calcium supplementation, urine potassium supplementation (dose: 0.1~0.3g/kg, concentration not exceeding 0.3%)
Rehydration type: 541, 2:1 solution, Ringer's lotion
Supplemented with antibacterial and symptomatic treatment
Brucellosis
Brucellosis, also known as undued fever, is a natural foci disease caused by Brucella. Clinically, it is characterized by long-term fever, sweating, fatigue, muscle and joint pain, liver, spleen and lymph node enlargement.
etiology
Gram-negative bacilli, facultative intracellular parasitism; the most pathogenic brucellosis of melitensis
Slow growth; weak resistance, sensitive to commonly used physical and chemical disinfectants, will die after 20 minutes of damp heat at 60°C or ultraviolet rays
Epidemiology
Source of infection
More than 60 species of livestock, poultry and wild animals are known to be the hosts of brucellosis, and now infected animals are transmitted to humans.
way for spreading
Infection through skin and mucous membrane contact
Gastrointestinal and respiratory tract infections
Susceptible groups
The population is generally susceptible and highly infectious after illness
Special occupations such as shepherds, veterinarians, and breeders are easy to obtain
popular features
Global disease; mainly prevalent in pastoral areas; in my country, Cattle and Sheep strains are the main pathogens
Pathogenesis and pathology
Brucella invades the human body from the skin and mucous membranes, reaches the lymph nodes with lymph fluid, grows and reproduces within the cells, and forms local primary lesions.
Bacteria multiply in large numbers in phagocytes, causing the phagocytes to rupture and enter the lymph and blood circulation to form bacteremia.
The germs travel throughout the body with the blood and form multiple lesions
Pathogenic bacteria release small endotoxins, which can cause bacteremia, toxemia and sepsis
Chronic fibrosis, T lymphocyte granuloma
clinical manifestations
The incubation period ranges from 1 to 3 weeks, with an average of 2 weeks, and may last several months or more than a year.
Types
Acute infection (course within 6 months)
Slow onset, fever (39~40℃ wave-like fever), excessive sweating, fatigue, muscle and joint pain, testicular swelling and pain, etc. Enlargement of the liver, spleen, and lymph nodes is common, accompanied by headache, neuralgia, rash, etc.
Pregnant woman suffering from illness and miscarriage
Chronic infection (more than 6 months)
Systemic non-specific symptoms, similar to neuroinflammation and chronic fatigue syndrome
Organic injuries are more common in the skeletal-muscular system, such as large joint damage, tendon contracture, etc.
Laboratory tests and other tests
Peripheral blood picture
Low or normal white blood cell count, relative or absolute increase in lymphocytes
Pathological examination
Cell culture: Take blood, bone marrow, tissue, cerebrospinal fluid, etc. for cell culture. The acute positive rate is high.
Immunological examination (confirmation)
Plate agglutination test for primary screening
In vitro agglutination test SAT: increased more than four times
Complications and sequelae
blood system
Anemia, leukopenia and thrombocytopenia, thrombocytopenic purpura, aplastic anemia, and hemophagocytic syndrome
Eye
Optic neuritis, corneal damage, etc., often seen in chronic brucellosis
Nervous and mental system, cardiovascular system, motor system
other
Pregnant women suffering from brucellosis who do not receive antimicrobial treatment may lead to miscarriage, premature death, and stillbirth.
treat
acute infection
Symptomatic and general treatment
Pathogen treatment
Principle: Early, combined, adequate amount, and sufficient course of treatment
Adults and children over 8 years old: Xicycline is the first choice
Rifampicin and co-trimoxazole or rifampicin combined with an aminoglycoside for children under 8 years of age
Pregnant women can use rifampicin combined with co-trimoxazole
Complications: Consider using three or more drug treatments, and the course of treatment needs to be extended appropriately.
Popularity cerebrospinal meningitis
It's called meningitis for short. , is an acute purulent meningitis caused by Neisseria meningitidis. Its main clinical manifestations are severe high fever, frequent headaches, vomiting, skin and mucous membrane petechiae, ecchymosis, and meningeal irritation and swelling. In severe cases, sepsis, shock and brain parenchymal damage can often be life-threatening. In some patients, the disease can occur rapidly. lethal.
etiology
Neisseria meningitidis, also known as meningococci, is a Gram-negative, kidney-shaped diplococcus that is an obligate aerobe.
This bacterium has weak resistance and is extremely sensitive to dryness, heat and humidity, cold, sunlight, ultraviolet rays and general disinfectants. It easily autolyzes and dies in vitro; it is severely resistant to sulfa drugs.
Epidemiology
Source of infection
Carriers and meningococcal meningitis patients are the main sources of infection, and humans are the only natural hosts of this bacterium. The significance of carriers as the source of infection is more important
way for spreading
It is mainly spread directly from the respiratory tract through droplets through coughing and sneezing.
Susceptible groups
The population is generally susceptible, and the silent infection rate of this disease is high
popular features
There will be peak incidence in winter and spring
Pathogenesis and pathology
Pathogenesis
Invading the human body from the nasopharynx, endotoxin released by bacteria is the main cause of this disease. Endotoxin causes Schwarzman reaction throughout the body.
Bacteria invade the meninges, enter the cerebrospinal fluid, and release endotoxins, causing purulent inflammation of the meninges and spinal cord and increased intracranial pressure.
pathological anatomy
The main lesion in the sepsis stage is vascular endothelial damage (petechiae)
In the meningitis stage, the main lesions are in the leptomeninges and arachnoids, and the cerebrospinal fluid is turbid.
subtopic
clinical manifestations
The incubation period is generally 1 to 2 days, with a maximum of 7 days.
Types
Common type (accounting for 90% of patients)
Prodromal stage (upper respiratory tract infection stage)
Low-grade fever, nasal congestion, sore throat
sepsis stage
High fever, chills, and body temperature rapidly rising to over 40°C, accompanied by obvious symptoms of systemic poisoning
Petechiae on the skin
meningitis stage
In addition to the symptoms of sepsis, high fever and poisoning, it is also accompanied by meningeal irritation symptoms such as severe headache, projectile vomiting, restlessness, neck stiffness, positive Kellniger sign and Bruzinski sign.
High fever, infection and poisoning symptoms, central nervous system symptoms
recovery period
Body temperature dropped, consciousness improved, and skin petechiae and ecchymoses healed. About 10% of patients develop perioral herpes
fulminant type
shock type
Symptoms of severe poisoning include sudden onset of chills, high fever, and in severe cases, the body temperature does not rise, accompanied by headache, vomiting, and petechiae and ecchymoses appear within a short period of time.
Rapid onset of circulatory collapse within 24 hours, disseminated intravascular coagulation (DIC)
Meningoencephalitis type
The main manifestations are damage to the meninges and brain parenchyma, with severe neurological symptoms appearing within 1 to 2 days; increased intracranial pressure, positive meningeal irritation signs, possible convulsions, and positive pyramidal tract signs.
Hybrid
Symptoms of shock and meningoencephalitis occur successively or simultaneously, and the mortality rate is extremely high
Lightweight
More common in the later stages, symptoms of upper respiratory tract infection such as low fever, mild headache and sore throat
chronic type
It is rare and more common in adults. The condition can last for weeks or months and often manifests as indirect chills and fever. After each attack, rashes or scars often appear in batches. leukocytosis
Laboratory and other tests
Blood
The total number of white blood cells increased significantly, and neutrophils increased above 80% to 90%. Thrombocytopenia in patients complicated with DIC
cerebrospinal fluid examination
It is an important method for diagnosis. Specimens should be sent for examination in time, kept warm, and checked in time.
Increased pressure, rice soup-like or pus-like appearance, increased white blood cells, mainly multinucleated cells; significant reduction in sugar and chloride, and increased protein content
cell culture
Complications and sequelae
complication
Otitis media, septic arthritis, endocarditis, pericarditis, pneumonia, eye disease, etc. caused by secondary infection or lesion migration
sequelae
Hydrocephalus, subdural effusion, extremity necrosis, etc. caused by adhesion of the brain and surrounding tissues, may also cause paralysis, epilepsy, mental disorder, etc.
diagnosis
Epidemic cerebrospinal meningitis is a purulent inflammation, and Japanese encephalitis is a degenerative inflammation.
Japanese encephalitis is more common in older children, in summer and autumn, with severe brain parenchymal damage (common in coma and shock), without petechiae, and clear appearance of cerebrospinal fluid, sugar =/piece, chloride =
Confirmed pathological cases
On the basis of clinical diagnosis, bacteriological or meningitis-specific serological immunological tests are positive
treat
normal type
Penicillin, cephalosporin or chloramphenicol is preferred
Treatment of intracranial hypertension and dehydration
fulminant shock type
Correction of DIC: Heparin
prevention
Sulfamethoxazole drug prophylaxis
Typhoid fever
Typhoid fever is an acute intestinal infectious disease caused by Salmonella typhi. Clinical features include persistent fever, apathetic expression, relative malaise, rosy rash, hepatosplenomegaly, and low white blood cells (proliferative reaction of the systemic mononuclear phagocyte system).
etiology
Salmonella typhi, Gram-negative, can grow in ordinary media, but grows better in bile-containing media
Does not produce exotoxins. Endotoxins play an important role in pathogenesis. They last longer in nature and are resistant to low temperatures.
Epidemiology
Source of infection
The carrier or patient is the only source of infection
way for spreading
fecal-oral transmission
Contaminated water sources are the most important route of transmission of this disease and can often cause outbreaks.
Food contamination is the main route of transmission
Close contact in daily life is the route of transmission of sporadic epidemics. Vectors such as flies and cockroaches can mechanically carry typhoid bacilli to cause sporadic epidemics.
Susceptible groups
Individuals who have never had typhoid fever and have not been vaccinated are generally susceptible. They can acquire relatively stable immunity after the onset of the disease, and a second attack is rare.
Pathogenesis and pathology
Whether or not the disease develops depends on the amount of bacteria ingested, their pathogenicity, and the host's defenses. Typhoid bacilli are quickly killed when the pH of gastric acid is <2
Activated macrophages play an important role in the intracellular killing mechanism of Salmonella typhi.
Macrophages phagocytose typhoid bacilli, red blood cells, lymphocytes and cell debris called typhoid cells. Typhoid cells aggregate into clumps and form nodules, becoming typhoid nodules or typhoid granulomas
Salmonella typhi that has not been killed by gastric acid invades the intestinal mucosa, and part of it enters the bloodstream through lymphatic vessels, causing the primary bacteremia stage (no clinical symptoms) → the bacteria multiply in the liver, spleen and other organs and then enter the bloodstream again, causing a second bacteremia Hyperemia (fever, hepatosplenomegaly, roseola; positive blood culture) → Bacteria multiply in the biliary tract and then enter the intestine to cause Arthus reaction (necrosis, ulcer, perforation), part of which is excreted in the urine → then gradually recovers
pathology
Systemic proliferative reaction of the mononuclear-macrophage system (especially collections/isolated lymphoid follicles in the terminal ileum)
clinical manifestations
incubation period
Usually 7~14 days
Typical clinical manifestations of typhoid fever
Early stage (first week)
The onset is slow, with fever symptoms appearing at the earliest. Fever is preceded by chills, and chills are rare. The fever rises in a stepwise manner, reaching a peak in 3 to 7 days, reaching 39 to 40°C. It is accompanied by general weakness, headache, dry cough, and loss of appetite. , nausea, abdominal pain, etc. Mild tenderness in the right lower abdomen, enlarged liver and spleen
Peak period (2nd to 3rd week)
Persistent fever: mostly residual fever type, lasting 1 to 2 weeks
Symptoms of nervous system poisoning (typhoid face): indifferent expression, sluggishness, unresponsiveness, tinnitus, hearing loss, delirium, stiff neck (a manifestation of asthenia meningitis) or even coma in severe cases
Circulatory system symptoms (relatively slow pulse): The heart rate does not increase with the increase in body temperature, but it is not obvious when it is complicated by myocarditis.
Digestive system symptoms: Half of the patients may have dull abdominal pain, located on the right side or diffuse, constipation is common, and there may be deep tenderness in the right lower abdomen.
Hepatosplenomegaly: proliferative reaction of monocyte-macrophage system.
Roseola: Small, light red maculopapular rashes appear on the 7th to 14th day of the disease, with a diameter of 2 to 4 mm, and fade when pressed. There are more than 10 rashes, distributed on the chest, abdomen, shoulders and back. It usually darkens and disappears in 2 to 4 days, and appears in batches.
Remission period (4th week)
Body temperature gradually drops, and neurological and digestive system symptoms weaken
Recovery period (week 5)
The body temperature is normal, neurological and digestive system symptoms disappear, and the liver and spleen return to normal.
Other types
Lightweight
Symptoms of systemic poisoning are mild, the course of the disease is short, and symptoms can return to normal in 1 to 2 weeks. More common in children or in early stages of disease
fulminant type
Acute onset, severe symptoms of toxemia, high fever or failure to rise in body temperature, complicated by toxic encephalopathy, myocarditis, shock, etc.
protracted
Fever lasts for more than 5 weeks to several months, with flaccid or intermittent fever, and obvious hepatosplenomegaly.
Carefree type
in special clinical settings
Typhoid fever in children
senile typhoid fever
rekindle
During the remission period, the body temperature does not drop to normal but then rises again, and the fever subsides after 5 to 7 days.
relapse
Some patients treated with chloramphenicol have clinical symptoms reappear 1 to 3 weeks after the fever subsides; this is related to the fact that the bacteria in the lesions are not completely removed and re-invade the blood stream.
Laboratory and examination
Blood routine
WBC↓with neutrophils and eosinophils↓; the absolute eosinophil count has reference value for the diagnosis and prognosis of typhoid fever
Bacterial culture
blood culture
The basis for diagnosis is that it can be positive at an early stage, and the positive rate is high within 1 to 2 weeks. Positive results may occur during relapse and relapse
bone marrow culture
The positive rate is higher; especially suitable for those who have been treated with antibacterial drugs, have a long course of disease and have negative blood culture
Stool culture
The positive rate is high in the later period, and the main value is to find carriers
Serum test (immunological test)
widal test
Principles and methods
The agglutination titer of the corresponding antibodies in the patient's serum is determined using the 0 antigen and H antigen of Salmonella typhi, and the H antigens of Paratyphi A, B, and C (5 types in total); Anti-O antibodies are of the IgM type, appear early and last for a short time; anti-H antibodies are of the IgG type, appear late and last for a long time
result
It is positive when the antibody titer is O≥1:80 and H≥1:160 (double serum antibody titer is more than 4 times higher than those with more reference value)
Complications and sequelae
Intestinal bleeding
Intestinal perforation
most serious complication
Toxic hepatitis, myocarditis, other complications bronchitis and pneumonia
diagnosis
Laboratory basis
Blood and bone marrow culture are of diagnostic significance, peripheral leukocytes are reduced, lymphocytes are relatively increased, and Feida test is positive to aid diagnosis.
treat
General treatment
The digestive tract is isolated until symptoms disappear and weekly stool examinations and 2 consecutive negative stool cultures are performed.
medical treatement
Fluoroquinolones (preferred drug): The course of treatment is 10 to 14 days; however, it is not suitable for pregnant women, children, and lactating women.
Cephalosporins: The third generation is suitable for pregnant women, children, lactating women, and fluoroquinolone resistance
prevention
Close contacts will be under medical observation for 15 days
scarlet fever
Scarlet fever is an acute respiratory infectious disease caused by group A beta streptococci. Its clinical features are fever, angina, diffuse bright red rash all over the body, and obvious desquamation after the rash.
etiology
Group A beta-hemolytic streptococci, also known as Streptococcus pyogenes, positive Gram stain
Lipoteichoic acid LTA has a high affinity for biofilms and helps streptococci adhere to human epithelial cells.
The pathogenicity comes from the bacteria themselves and the toxins and proteases they produce.
toxins produced
Pyrogenic exotoxins, hemolysins
Protease produced
Streptokinase (fibrinolytic protease), hyaluronidase (diffusion factor), streptokinase (deoxyribonuclease), nicotinamide adenine dinucleotidase, serum turbidity factor (an alpha protease)
Epidemiology
Source of infection
Patients and carriers are the main sources of infection (especially patients with anginositis caused by streptococci)
way for spreading
Mainly spread through air droplets, but also surgical or obstetric scarlet fever caused by skin trauma and maternal birth canal
Susceptible groups
generally susceptible
popular features
More common in temperate zones and can occur throughout the year
Pathogenesis and pathology
purulent lesions
Streptococci adhere to mucosal epithelial cells with the help of LTA, invade tissues and cause inflammation.
toxic lesions
The toxins produced by Streptococcus enter the blood circulation and cause systemic toxemia
allergic disease
clinical manifestations
The incubation period is 1 to 7 days, usually 2 to 3 days
Types
normal type
Most patients belong to this type
Fever, mostly persistent, body temperature can reach 39°C, accompanied by systemic poisoning symptoms such as headache, general malaise, etc.
Angina: manifests as sore throat, odynophagia, local congestion with purulent exudate, and non-purulent inflammatory changes in submandibular and cervical lymph nodes
Rash: The rash begins 24 hours after fever, starting behind the ears, neck and upper chest, and then quickly spreads throughout the body; the typical rash is a diffuse congestive pinpoint-sized rash evenly distributed on the skin, which fades under pressure and is accompanied by itch. Some patients have a rash called "milia" with yellowish-white pus heads that are not easy to break. Some cases include linear rash (Paaskin's lines), strawberry tongue, and bayberry tongue.
After the rash recedes, desquamation begins, with miliary rash being the most severe.
septic type
Rarely, malnourished children. Purulent inflammation in angina
Poisoning type
Toxemia is obvious and the mortality rate is high and rare. High fever, headache, severe vomiting, confusion, toxic myocarditis and septic shock
Surgical/Obstetrical
Pathogens invade from wounds or birth canals. There is no angina. Symptoms are generally mild and the prognosis is good.
Laboratory and other tests
Blood
Leukocytosis (10~20×10⁹/L), neutrophils above 80%, eosinophilia after rash may account for 5% or 10%
serology test
Fluorescence detection of throat swab smears
Pathological examination
Culture of throat swabs or secretions from other lesions for hemolytic streptococci
diagnosis
treat
General treatment
respiratory isolation
Pathogen treatment
Penicillin, erythromycin or compound sulfamethoxazole for allergies
Symptomatic treatment
For septic toxic shock, actively replenish blood volume, correct acidosis, and give vasoactive drugs
For suppurated lesions, timely incision and drainage or surgery
bacillary dysentery
Bacillary dysentery, referred to as bacillary dysentery, is an intestinal infectious disease caused by Shigella. It is mainly spread through the digestive tract and is popular in summer and autumn. Pathological changes include inflammation and ulceration of the rectum and sigmoid colon. The main manifestations are abdominal pain, diarrhea, mucus, pus and blood in the stool, and tenesmus. It may be accompanied by fever and systemic toxemia symptoms. In severe cases, septic shock may occur.
etiology
Shigella, commonly known as Shigella dysenteriae, a gram-negative bacillus
Antigen structure
Shigella bacteria are divided into 4 serotypes or subtypes. In my country, Shigella flexneri and Shigella sonnei are dominant
resistance
Exists in the feces of patients and carriers, and has weak resistance
toxin
Endotoxins and exotoxins (Shigella toxins)
Epidemiology
Source of infection
Including patients with acute and chronic bacillary dysentery and carriers
way for spreading
Mainly transmitted through feces-oral
population susceptibility
generally susceptible
popular features
developing country
Pathogenesis and pathology
Pathogenesis
Number of bacteria
Pathogenicity
body resistance