can tuberculosis affect liitle children? if so what are its symptoms?

Answer 1

TB can affect anyone. It is highly contagious. You can be exposed and not get sick, though. Whether or not one gets sick usually depends on one's general health, which is why TB is rampant in third world countries with poor nutrition and hygiene.

TB can be treated with a long (6 months or more) treatment with multiple antibiotics like isoniazid and rifampin. However, there are strains emerging that are resistant to multiple drugs.

No vaccines for the general population are currently used in the US, but are available in other countries. The effectiveness of these vaccines is disputed.

Symptoms:
A cough with thick, cloudy, and sometimes bloody mucus from the lungs for more than 2 weeks.
A rapid heartbeat.
A swollen neck (when lymph nodes in the neck are infected).
Fever, chills, and night sweats.
Fatigue and muscle weakness.
Loss of appetite and unexplained weight loss.
Shortness of breath and chest pain (in rare cases).

Answer 2

Of course it can and is usually a primary complex. On x-ray, the result is calcified hilar nodes and a Ghon tubercle in the lower of middle lobe with calcification. A year of treatment is indicated. OT test is positive.

Answer 3

tuber culosis, is a disease called by bacteria it invades the lungs, yes it can infect children and the main symptoms r short breath, fever and a violent cough, but when born most children get a vaccine so u've gotta check this

Answer 4

tb can affect anyone, the main symptoms are fever and night sweating, have it checked out by a doctor if you suspect, a simple xray will determine

Answer 5

I think so, but not positive. You best ask a doctor.

Answer 6

only if the patient has a uterus, ovaries, and other parts necessary for childbirth. discuss the concerns with your OB.

Answer 7

yes,weight loss,cachecsia,cough,positive fammilial history.

Answer 8

here is a website it tell you everything.

Answer 9

Tuberculosis remains one of the major diseases afflicting children throughout the world. Although the exact number of annual cases of childhood tuberculosis is unknown, the World Health Organization (WHO) has estimated approximately 1 million new cases and 400,000 deaths per year in children due to tuberculosis.[1] Many of these cases go undiagnosed and untreated and many of these children could be salvaged if there were improvements in diagnosis and treatment available for children.

Many experts in childhood tuberculosis feel that children have been neglected in the worldwide effort to control tuberculosis. There are many reasons for this including the fact that most children with tuberculosis are not infectious and therefore not considered to be as important as adults with contagious tuberculosis, the frustration at the difficulty in establishing a microbiological diagnosis of tuberculosis in children, and the relative neglect of pediatricians and researchers in studying childhood tuberculosis.[2] In fact, there is a rich scientific literature about childhood tuberculosis supporting simple practices, which, if adequately put into place, would greatly improve the ability to diagnose and treat children with tuberculosis.
Tuberculosis remains one of the major diseases afflicting children throughout the world. Although the exact number of annual cases of childhood tuberculosis is unknown, the World Health Organization (WHO) has estimated approximately 1 million new cases and 400,000 deaths per year in children due to tuberculosis.[1] Many of these cases go undiagnosed and untreated and many of these children could be salvaged if there were improvements in diagnosis and treatment available for children.

Many experts in childhood tuberculosis feel that children have been neglected in the worldwide effort to control tuberculosis. There are many reasons for this including the fact that most children with tuberculosis are not infectious and therefore not considered to be as important as adults with contagious tuberculosis, the frustration at the difficulty in establishing a microbiological diagnosis of tuberculosis in children, and the relative neglect of pediatricians and researchers in studying childhood tuberculosis.[2] In fact, there is a rich scientific literature about childhood tuberculosis supporting simple practices, which, if adequately put into place, would greatly improve the ability to diagnose and treat children with tuberculosis.

Other radiographic findings occur in some patients. Occasionally, children have a picture of lobar pneumonia without impressive lymphadenopathy. If the infection is progressively destructive, liquefaction of the lung parenchyma leads to formation of a thin-walled primary tuberculous cavity.[39] Rarely, bullous lesions occur in the lungs leading to pneumothorax.[40] Enlargement of the subcarinal lymph nodes causes compression of the esophagus, and rarely, bronchoesophageal fistula. A sign of subcarinal tuberculosis is horizontal splaying of the mainstem bronchi.

Older children and adolescents can develop the more typical adult type reactivation tuberculosis.[41-43] They are more likely to experience the classic symptoms of fever, anorexia, malaise, weight loss, night sweats, productive cough, chest pain, and hemoptysis than younger children. However, findings on physical examination are usually minor or absent even when cavities or large infiltrates are present. Most signs and symptoms improve within several weeks of starting effective treatment although cough may last for several months. In these cases, the chest radiograph appearance is that typically seen in adults with a predominance of upper lobe infiltrates with or without cavitation. Some adolescents get a somewhat peculiar form of tuberculosis resulting in necrotizing pneumonitis. In these cases, it can be difficult to establish the diagnosis of tuberculosis because the sputum is often devoid of organisms; in my experience, open lung biopsy has been required in several cases to establish the correct diagnosis.

Extrapulmonary Tuberculosis
A complete review of extrapulmonary tuberculosis in children is beyond the scope of this monograph. For most forms of extrapulmonary tuberculosis, the clinical presentation is similar in children to that in adults. However, there are two forms of extrapulmonary tuberculosis that are common in children and merit special attention. The first is lymphohematogenous disease.[44] Tubercle bacilli are disseminated to distant sites in all cases of tuberculosis infection. This dissemination is clinically silent in most cases but can be the origin of miliary tuberculosis or extrapulmonary tuberculosis in the immediate or distant future. Other patients experience protracted hematogenous tuberculosis caused by an intermittent release of tubercle bacilli as a caseous focus erodes through the wall of a blood vessel in the lung. Although the clinical picture may be acute, more often it is indolent and prolonged, with spiking fevers accompanying the release of organisms into the bloodstream. Multiple organ involvement is common leading to hepatomegaly, splenomegaly, and lymphadenitis in superficial or deep nodes. Early pulmonary involvement is surprisingly mild, but diffuse lung involvement becomes apparent if treatment is not given promptly. Culture confirmation of this form of tuberculosis can be difficult, often requiring sampling of the bone marrow or liver biopsy with the appropriate stains and cultures.

The most common clinically significant form of disseminated tuberculosis is miliary disease, which occurs when massive numbers of tubercle bacilli are released into the bloodstream causing disease in two or more organs.[45-47] Miliary tuberculosis usually occurs early after the infection, within the first 2 to 6 months. The clinical manifestations of miliary tuberculosis are protean, depending on the load of organisms and where they lodge. Lesions are usually larger and more numerous in the lungs, spleen, and bone marrow than other organs. This form of tuberculosis is most common in infants and in malnourished or immunosuppressed patients. The onset of clinical disease is sometimes explosive and the patient may become gravely ill in several days. More often, the onset is insidious; the patient may not be able to pinpoint accurately the time of onset of the initial symptoms. Early systemic signs include malaise, anorexia, weight loss, and low grade fever. Within several weeks hepatosplenomegaly and generalized lymphadenopathy develop in about one half of cases. About this time, the fever may become higher and more sustained although the chest radiograph usually remains normal and respiratory symptoms are few. Within several weeks, the lungs become filled with tubercles, and dyspnea, cough, rales, or wheezing occur.[48] As the pulmonary disease progresses, an alveolar air block syndrome may result in respiratory distress, hypoxia, and pneumothorax or pneumomediastinum. Signs or symptoms of meningitis or peritonitis are found in 20 to 40% of patients with advanced disease. Cutaneous lesions such as papulonecrotic tuberculosis often appear in crops.[49] Choroid tubercles occur in 13% to 87% of patients and are highly specific for tuberculosis.

The second form of extrapulmonary tuberculosis that is particularly common among children is tuberculosis of the central nervous system, most commonly meningitis.[50-54] Tuberculous meningitis is the most serious complication in children and is uniformly fatal without treatment. The brain stem is the most common focus; cranial nerves III, VI, and VII are frequently involved.[55] The condition arises from the formation of a metastatic caseous lesion in the cerebral cortex or meninges that develops during the occult dissemination of the primary infection. This lesion, called a Rich focus, increases in size and discharges small numbers of tubercle bacilli into the subarachnoid space.[55] The resulting gelatinous exudate may infiltrate the cortical or meningeal blood vessels producing inflammation, obstruction, and infarction of the cerebral cortex. The exudate also interferes with the normal flow of cerebrospinal fluid (CSF) in and out of the ventricular system at the level of the basal cisterns leading to a communicating hydrocephalus. The combination of vasculitis, infarction, cerebral edema, and hydrocephalus results in this severe damage that can occur gradually or rapidly.

The clinical progression of tuberculous meningitis may be rapid or gradual. Rapid progression tends to occur more often in infants who may experience symptoms for only several days before the onset of acute hydrocephalus, seizures, or cerebral edema. More often, the signs and symptoms progress slowly over several weeks and can be divided into three general stages. The first stage, which typically lasts 1 to 2 weeks, is characterized by nonspecific symptoms such as fever, headache, irritability, drowsiness, and malaise. Focal neurological signs are absent but infants may experience stagnation or loss of developmental milestones. The second stage often begins abruptly with lethargy, nuchal rigidity, and Kernig's or Brudzinski's signs, seizures, hypertonia, vomiting, cranial nerve palsies, and other focal neurological signs. This clinical picture usually correlates with the development of hydrocephalus, increased intracranial pressure, and vasculitis. The third stage is marked by coma, hemiplegia or paraplegia, hypertension, decerebrate posturing, deterioration in vital signs, and, eventually, death. The prognosis of tuberculous meningitits correlates most closely with the clinical stage of illness at the time antituberculosis chemotherapy begins.[56] The majority of patients in the first stage have an excellent outcome, whereas most patients in the third stage who survive have permanent disabilities including blindness, deafness, paraplegia, and mental retardation.[57]