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Infectious Diseases 1
Infectious disease
 Infectious diseases are a group of diseases caused by
pathogenic organisms and can be epidemic among
certain population.
 Necessary factors for transmission of infectious disease
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•
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Source of transmission 传染源
Routes of transmission 传染途径
Susceptible host 宿主
 Epidemiology: infectious disease is a public condition associated
with the socioeconomic conditions. 发展中国家？
 The organisms producing diseases in human are various.
 Major histologic patterns of tissue reaction in infections
 suppurative inflammation
 mononuclear and granulomatous inflammation
 necrotizing inflammation
 chronic inflammation and scarring
Tuberculosis 结核病
This is the chronic, communicable disease caused by
mycobacterium tuberculosis.
Tuberculosis is estimated to affect 1.7 billion individuals
worldwide, with 8 to 10 million new cases and 1.7 million
deaths each year.
After HIV, tuberculosis is the leading infectious cause of
death in the world. Infection with HIV makes people
susceptible to rapidly progressive tuberculosis; over 50 million
people are infected with both HIV and M. tuberculosis.
1.Etiology and pathogenesis:
The common human strain infects only humans. Patients with
pulmonary tuberculosis who cough up bacilli in the sputum are
the source of transmitted infections. 痰
The bovine strain of M. tuberculosis infected dairy, causing
human infection via contaminated milk. Bovine tuberculosis
typically involved the oropharynx or intestine because the
organism was ingested in milk.
Components of the M. tuberculosis cell wall (such as
cold factor, wax D, complement, heat-shock protein, etc ) and
host response(immune response and delayed hypersensitivity)
contribute to its pathogenicity.454
2. Basic pathological changes
Exudative changes dominate 渗出
— Early infections, numerous mycobecteria, high
bacteria virulence, low host immunity and pronouned
hypersensitivity.
— Serous membrane, synovium, meninx and lung.
— Serous or sero-fibrinous inflammation.
 Proliferative changes dominate 增生-结核结节
— Few organisms, low virulence and high host immunity.
—The tubercle-the most characteristic changes in tuberculosis.
Typical tubercle (tuberculous granuloma) consists of caseous
necrosis in the center,surrounding it by the epithelioid and some
Langhan’s giant cells,with a peripheral aggregation of small
Lymphocytes and fibroblasts.
The tubercle can be isolated or fuse to a large one.
 Necrotic changes dominate 干酪样坏死
—Numerous organisms, high bacteria virulence, low host immunity
and strange hypersensitivity reaction.
—Extensive caseous necrosis
Gross : pale yellowish or creamy-white in color,soft and friable,
similar to dry cheese.
Microscopically: red strained homogeneous amorphic material with
cell debris sometimes or slightly granular material
Caseous necrosis is equal diagnostic importance in TB.
Large areas of caseous necrosis are a sign of TB progression.
3. Conclusion :
—The lesions of tuberculous infection depends on the interaction
between the organism and the host(the infecting host, virulence
of the organism, the degree of immunity or resistance , and
hypersensitivity of the host) .
—These three basic pathological changes can also interchange
according to host conditions. Hence the disease may be manifest
different. 变质、渗出、增生
4. Fate of the tuberculosis
 Healing of tuberculosis lesion 愈合
— Absorption and resolution. 吸收消散
— Fibrosis, fibrous encapsulation and calcification of
lesions. 纤维化、纤维包裹及钙化
 Exacerbation of tuberculous lesions 恶化
— Infiltration and progression. 浸润进展
—Dissolution and dissemination. 溶解消散
5. Pulmonary tuberculosis 肺结核
The lungs are the most commonly affected by tuber- culosis
than any other organs.
The pattern of host response depends on whether the
infection represents a primary first exposure to the organism or
secondary reaction in an already sensitized host. 原发、继发
456
Ⅰ.Primary pulmonary tuberculosis
This form occurs when child who has not been previously
exposed to tuberculous bacillus or immunised by BCG. So
called the childhood type TB, but primary lesion may also
occurs in adult at a low rate of the tuberculosis.
 Pathology
Primary complex (the Ghon complex).
The lesion consists of three components
— Primary lesion (Ghon focus).
— Tuberculous lymphangitis.
— Tuberculous lymphadenitis (in the hilar lymph nodes).
Clinical features
Primary pulmonary tuberculosis is usually
asymptomatic or manifested as a mild flu-like illness.
The fate of primary pulmonary TB
—In 95% of cases, immunity stops disease progression and
healing occurs. The lesions heal by fibrosis and may calcify.
—In 5% of cases, rapidly progressive pulmonary disease
causing extensive caseous consolidation of the lung, usually
occurs only in malnourished or immunodeficient children.
Ⅱ. Acute pulmonary milliary tuberculosis
Caseous necrosis in the hilar lymphadenopathy escape
into a systemic vein, either directly or by involvement of the
thoracic duct, and via right heart, pulmonary artery,
disseminating to the lung.
Ⅲ. Acute systemic miliary tuberculosis
Hematogenous disseminated lesions of pulmonary TB

Large numbers of mycobacteria enter usually one of the
pulmonary veins, via left heart, into the arterial systemic
circulation and spreading to the general various organs.

Gross: multiple,scattered, too small(approximate 1-2mm in
diameter), fairly uniform size, round, gray white well
demarcated nodules.

Microscopically: proliferative changes dominate(formation
tubercle, often without giant cells, but with central necrosis.

Clinical symptoms: high fever, night sweats, loss of appetite,
failure, hepatomegaly and splenomegaly.
Ⅳ、Second pulmonary tuberculosis 继发性肺结核
Secondary pulmonary TB is occurrence of the disease
in a patient who has a prior primary infection. It usually
occurs in an adult as a result either of reinfection or
reactivation,with the latter more common. 内源性
Secondary tuberculosis,however,tends to produce more
damage to the lungs than does primary tuberculosis. 肺部
The subsequent course of the secondary lesions is
variable.
①Focal pulmonary tuberculosis 局灶性肺结核
 The earliest lesions.
 The most common site is the lung apex 肺尖, one or more
small focus of consolidation.
 Small epithelioid cell granulemas characterized by caseous
necrosis and fibrosis.
 Usually asymptomatic.
They either may heal spontaneously or with therapy,
resulting in a fibrocalcific nodule 钙化点.
②Infiltrative pulmonary tuberculosis 浸润型肺结核
This is a most common form in the second pulmonary tuberculosis
and usually transformed from focal pulmonary TB.
This is a activity pulmonary TB.
The heavy exudation and caseous necrosis continue to appear at
the periphery focal tuberculous lesion and to cause the lesion
enlargement.
Complication: irregular acute cavities.空洞
spontaneous pneumothorax. 气胸
tuberculosis pyopneumothorax. 脓胸
Clinic features: tuberculous toxic symptoms and chronic cough,
frequently with hemoptysis.
③Chronic fibro-cavitative pulmonary TB 慢纤空
This is a most common form of chronic pulmonary TB in an adult.
Pathological changes :
•It may affect one, many or all lobes of both lungs.
•The upper lobes of lung contains multiple variant sizes, thick-walled chronic
cavities.
•The wall of cavity is lined by a yellow-green caseous material, tuberculous
granulation tissue and fibrous tissue successively.
•There may be coexisting bronchial disseminated many tuberculous
lesions and diffuse fibrosis in the pulmonary tissues.
•Later period, the lung becomes small, indurated,with pleural extensive
adhesion, the function of the lung may be severely damaged.
④ Caseous pneumonia 干酪性肺炎
May occur in debilitated
immunodeficient or highly sensitized
patients.
Dissemination large numbers of
organisms in the focus via the
bronchial tree,and spreading rapidly
throughout large areas of lung
parenchyma and producing a diffuse
bronchopneumonia or lobar exudative
consolidation
⑤ Tuberculoma 结核球
The caseous necrosis coalescence to
form a large solid and spherical mass
(usually 2-5cm in diameter), welldemarcated margin, surrounded by
fibrous tissue. 与肺癌鉴别
⑥ Tuberculosis pleuritis 结核性胸膜炎
According affected feature divide into:
湿性Moist tuberculous pleuritis (exudative tuberculous pleuritis)
• This is a exudative inflammation dominate(serious or serofibrinous).
• Heave serious liquid→hydrothorax. 胸水
heavy fibrin formation→thoracalgia.
干性Dry tuberculous pleuritis (proliferative tuberculous pleuritis)
• This is a proliferative lesion dominate.
• Localized tubercles may form in the visceral pleura, and this may be followed
by an tuberculous focus beneath pleura.
6. The extrapulmonary tuberculosis 肺外结核
A relatively small number of mycobacteria gain entrance
the bloodstream (capillary vessel of primary focus) and
may be formed latent lesion in the extrapulmonary organs,
causing extrapulmonary tuberculosis such as meningitis
and tuberculomas of brain, vertebral tuberculosis, renal
tuberculosis, intestinal tuberculosis. 脑、骨、肾、肠
Typhoid fever
伤寒 464
Typhoid fever is an acute infectious disease caused by
salmonella typhi 伤 寒 沙 门 菌 with hyperplasia of
mononuclear-macrophages in the reticuloendothelium of all
over the body 全身单核巨噬细胞系统(intestinal and the
mesenteric lymph nodes, liver, spleen and bone marrow, etc)
and corresponding clinic features.
1.Etiology and pathogenesis
Pathogen
•S typhi is a facultative intracellular organism and infects only humans.
endotoxin(strong pathogenicity).
without exotoxin.
•Somatic antigen(“o”antigen).
•Flagellar antigen(“H” antigen)→serum agglutination.
•Surface antigen (“V1“ antigen)
test(wildal’s test).肥达反应
Source of infection —patients and healthful carriers.健康携带者
Routes of infection —fecal-oral transmission. 粪口传染
The infection results from contamination of food and water with
feces from a symptomatic case or a symptomatic carrier of typhoid.
The files are important vectors. 苍蝇
Pathogenesis
1. The ingested bacillus invades the small intestinal mucosa, where it
is taken up by macrophages and transported to regional lymph nodes
and multiplies in the intestinal lymphoid tissue during the ten days
incubation period.
2. At the end of the incubation period, the bacilli enter the
bloodstream (endotoxaemia and bacteremic phase, in the first week),
resulting in fever headache and muscle aches 肌肉痛. Many tissues
may be infested during this phase, blood culture is positive in 95%
of case.
3. S typhi reenters the intestinal lumen by way of biliary excretion.
The organism reinfects lymphoid tissue in the small intestine causing
acute inflammation, necrosis and ulceration (organism direct invasion,
endotoxin released by the bacillus, together with delayed
hypersensitivity).
Stool and urine culture is positive at this stage
blood culture is still positive in about 60% of pationts
widal’s test is positive.
4. Healing usually begins’ about the end of the third week and is
complete by the fifth week in uncomplicated cases.
2.Pathology and clinical features
Acute hyperplastic inflammation(hyperplasia of the
mononuclear-macrophages). 增生性炎症
The hyperplastic mactophages ingest bacteria, red cells
and nuclear debris tend to form a small nodule in lymphoid
tissue, such nodule is caused typhoid granuloma and the
macrophage is called typhoid cells.伤寒肉芽肿 、伤寒细胞
Ⅰ.Intestinal lesion 肠伤寒
*Location—terminal ileum and caecum. 回肠末端
*Lymphoid tissue in intestine tract—usually most marked in the
Peyer’s patches of the distal ileum and solitary lymphoid follicles
of the caecum.
Ⅰ.Intestinal lesion
—The stage of medullary swelling (the first week) 髓样肿胀期
Gross: the lymphoid patches initially show an inflammatory swelling and enlargement correspond
I shape and extent to the lymphoid patches.
Microscopically: the lymphoid patches show congestion, edema, marked proliferation of
macrophage and typhoid granuloma formation.
Clinic: becteraemia is accompanied by progressive fever, sometimes with a staircase-like rise.
—The stage of necrosis (the second week) 坏死期
The necrosis extends deeply to involve the muscular propria
and even the serosal coat.
The development of focal necrosis can lead to softening and
rupture of the lymphoid patches.
Clinic: 5/6 persistent high fever.
bradycardia.
hepatosplenomegaly.
rose—coloured spots in the skin.
leukocytopenia.
diarrhea.
—The stage of ulceration (the third week) 溃疡期
The mucosal ulcers tend to take the shape and extent of the
underlying lymphoid patches (round or oval), and typically occur
as longitudinal ulcers overlying the peyer patches in the ileum.
Clinic: the general symptoms remission of patients.症状缓解但
小心穿孔
—The stage of healing (the fourth week) 愈合期
Healing of these ulcerated lesions leaves a smooth scar which
never shows any tendency towards stricture formation. 无狭窄
Clinic: the temperature shows a staircase-like descend to recover
normal.
Ⅱ.Chages in other organ
Typhoid fever is associated with a great variety of lesions
which are widely distributed and may arise during the course
of the disease or later: they are due to endotoxaemia and
bacteraemia.
3.complications 并发症
•Severe hemorrhage may occur from the intestinal ulcers.
•A more serious complication resulting from extensive necrosis
is perforation of the small vowel with usually fatal generalized
peritonitis. 肠穿孔、腹膜炎
•Development of laryngitis, bronchitis and bronchopneumonia
may be due to invasion by other bacteria. 支气管性肺炎
Bacillary dysentery 细菌性痢疾
Bacillary dysentery — an acute pseudomembranous inflammation
caused by shigella species and a common intestinal infectous disease.
1.Etiology and pathogenesis
• Pathogen — Shigella species, gram-negative bacilli.
The four species of Shigella are pathogenic for humans
*Shifella sonnei
*Shigella flexneri
the common species and cause a relatively
mild illness
*Shigella boydii—uncommon
*Shigella dysenteriae—produces a severe illness
Source of infection —patients and healthful carriers.
Routes of infection — atypical fecal — oral transmission.
transmitted by food and water contaminated by shigella.
flies serve as an important vectors in transmission.
 Pathogenesis— the organisms invade directly the intestinal mucosa.
multiplication in the lamina propria and teleasing the toxin
Producing an acute inflammation and
Toxaemia
tissues injury
2.Pathology and clinical features
Location—sigmoid colon, rectum are the most commonly
affected area and in severe conclitions all the
colon and the terminal ileum can be affected 乙状结肠、直肠
① Acute bacillary dysentery 急性细菌性痢疾
Initial, acute catarrh inflammation—producing an acute inflammation with diffuse hyperemia, edema, punctuate hemorrhage,
infiltrating of inflammatory cells (neutrophils), excess mucus
secretion and formation superficial erosion in the mucosa
Follow, pseudomembranous inflammation—
*Pseudomembane is fibrinsuppurative exudate in nature
*Just on the surface of the mucosa of affected colon firstly the pseudomembrane
patchily distributed and then diffusely cover the mucosa and produce a dirty
membranous matter
*Under microscope, the pseudomembrane is composed of fibrins, numerous
neutrophils admixed with red cells, cell debtis and bacteria 粘液脓血便
*When the seudomembrane sheds, the irregular superficial ulcer
appears(maplike ulcers)
Later, the ulcers heal and the patients recover
① Acute bacillary dysentery
Clinic appearance
Toxaemia—fever, peripheral blood leukocutosis.
Inflammatory— abdominal cramping .
irritation
diarrhea with mucus, blood and pus in the stool.
Complication: hemorrhage.
perforation(less commonly).
dehydration.
electrolytic disturbance(in serious cases).
Fate: healing (most cases).
in some cases, protracted and pass into a chronic condition.
②.Chronic bacillary dysentery
Course of disease has been exceeded more than 2 months.
Such chronic cases are characterized by repeated injury and
repair, ulceration and healing, and can lead to new and old lesions
coexist, chronic ulcer formation, polypoid mucosal irregularity
with fibrous scarring and subsequent stenosis of the bowel.
Clinic appearance:
Abdominal pain, chronic diarrhea intestinal obstruction.
③. Toxic bacillary dysentery 中毒型
The most common in children.
Often from organism of lower virulence.
the onset of disease is sudden.
Intestinal lesion is child, showing catarrh enteritis or
follicular enteritis.
There are severe general toxic symptoms (high fever,
convulsion).
After onset some hours, toxic shock and coma or brain edema
and respiratory failure appear rapidly. 注意并发症