L. Miguel. Mount Marty College.
Zhongguo Zhen Jiu (Chinese Acupuncture & Moxibustion) 10: 23 24 (in Chinese with English abstract) 436 17 Beneficial Effect of Acupuncture on Depression Qiong Liu and Jin Yu Department of Integrative Medicine and Neurobiology Shanghai Medical College of Fudan University anastrozole 1mg with mastercard, Shanghai 200032 anastrozole 1 mg lowest price, P buy anastrozole 1 mg mastercard. China Summary This chapter presents the clinical and laboratory evidence regarding the effect of acupuncture on depression and its potential mechanisms. Most of the clinical studies have demonstrated that either acupuncture alone or acupuncture combined with other therapies has a therapeutic effect on subjects with depression. The adverse effects were less and milder in the group under acupuncture treatment than in those under regular medication. Lastly, the hippocampus, an important brain structure that plays a key role in the etiology of depression, has been observed to be involved in the mechanism of acupuncture. Psychologist Martin Seligman addressed depression as the “common cold” of psychological problems, because nearly everyone suffers from it at some time point. Clinical depression is a real medical condition and is different from the term “being depressed” that is used frequently. It is a “whole-body” illness, involving the body, mood, and thoughts, which presents with depressed mood, loss of interest or pleasure, feeling of guilt or low self-worth, disturbed sleep or appetite, low energy, and poor concentration. These symptoms linger, intensify, and lead to substantial impairments in an individual’s social functioning and/or activities of daily living. In other words, depression can interfere with a person’s normal functioning, and frequently disrupt the work, social, and family adjustment. It makes a person feel sad or hopeless most of the time and lose interest in things that were once enjoyed. It affects the way a person eats and sleeps, the way one feels about oneself, and the way one thinks about things. People who suffer from depression usually struggle to do even the simplest things. The economic cost for this disorder is high, but the cost of human suffering cannot be estimated. It causes pain and suffering not only to those who have the disorder, but also to those who care about them. Serious depression can destroy family life as well as the life of the depressed person. There are a variety of antidepressant medications and psychotherapies that can be used to treat depressive disorders. Psychological treatment of depression (psychotherapy) assists the depressed individual in several ways, which include supportive counseling, cognitive therapy, and problem-solving therapy. Some people with milder forms of depression may respond well to psychotherapy alone, while those with moderate to severe depression most often benefit from antidepressants. Most of the patients respond best to combined treatment: Medication—to gain relatively quick symptom relief, and psychotherapy—to learn more effective ways to deal with life’s problems, including depression. However, conventional treatments like psychotherapy and medication can alleviate the symptoms in a whopping 50% 70% of patients who complete the regimen; however, about one-third of the patients who begin therapy never complete it, because they may not observe any improvement or may experience debilitating side effects. Even among people who recover from depression, more than one-third revert back within 18 months. In addition, most empirically supported psychotherapies are also not readily available or affordable. Hence, there is a need for safe, effective, and affordable alternative treatments for depression. Acupuncture originated in China at least 3000 years ago, and moved to the west in the 1970s. It is a type of therapy that involves inserting needles into the acupoints along the body’s meridians. This chapter summarizes the therapeutic practice and mechanistic research on acupuncture treatment for depression. Some examples of typical clinical cases will be discussed in the following sections. Simultaneously, we will also list some of the commonly used acupoints for the treatment of depression. In these studies, either the primary or secondary depression has been addressed, although there are some studies without double-blinded control. These clinical data give us some indications that acupuncture can be utilized as a therapy for depression. A total of 440 patients with depressive neurosis, a subtype of depression, were employed in this study, and were divided into three groups: an acupuncture group, a non-acupoint needling group, a Prozac group. On the other hand, needling the points that deviate from the acupoints was prescribed for the non-acupoint group, as a control treatment. These results demonstrate more positive clues that acupuncture is an effective and safe therapy for depressive neurosis. The therapeutic effect of acupuncture on depressive neurosis is observed to be possibly better than or similar to fluoxetine, but with less side effects. Thus, the well- designed clinical trials carried out in multi-centers with strict control provided further evidence on the clinical applications of acupuncture. In 2007, another pilot study was published on the Chinese Journal of Integrated Traditional and Western Medicine (Zhongguo Zhong Xi Yi Jie He Za Zhi) (Li and Liu 2007). A total of 56 depressed patients (from mild to severe) were randomized into two groups: acupuncture group and medication group. Furthermore, the therapeutic effect appeared earlier and lasted longer in the acupuncture group than in the medication group. However, this study did not monitor the side effects of acupuncture and did not set up the sham-acupuncture control and double-blinded assessment systems. Nevertheless, this study further suggests that acupuncture could be a promising therapy for depression. Furthermore, a randomized controlled study focused on the female patients with climacteric depression, a subtype of secondary depression was carried out (Zhou and Wu 2007). A total of 60 cases were examined and randomly assigned to acupuncture group and medication group. As a control therapy, 20 mg/d of fluoxetine was administered to the medication group. Although the results imply that acupuncture can improve the climacteric depression, the clinical implications of acupuncture on this condition must be investigated further. On the other hand, the oral medication of fluoxetine (20 mg/d) was prescribed for the control group. In one study, 68 participants who did not take any mood-altering drugs (11 with anxiety, 8 with depression, and 49 with both anxiety and depression) were recruited to assess the impacts of acupuncture on anxiety and depression symptoms in patients with chronic disease (Tao 1993). The results showed a statistically significant reduction in both anxiety and depression, 1 month after acupuncture treatment. The first study was double-blinded placebo-controlled, in which 29 depressed inpatients were included. In addition, based on the results and research protocol of the previous study, a multi-centered collaborative study was conducted, in which 241 inpatients with depression were included. Particularly, it can be a beneficial choice for depressed patients who could not comply with the classic tricyclic antidepressants owing to their anticholinergic side effects. To further scientifically confirm the efficacy of acupuncture on depression and improve the clinical application, it is very important to carry out well-designed clinical trials of randomized controlled double-blinded protocol. The aim of this pilot study was to determine whether acupuncture holds promise as a treatment for depression during pregnancy. Standardized acupuncture treatments were individually tailored and provided in a double-blind fashion. All the responders to the acute phase of all the treatments had significantly lower depression scores at 10 weeks postpartum, than the non-responders. Thus, this study demonstrated that acupuncture is a promising technique for the treatment of depression during pregnancy. Each 8-week intervention regimen consisted of 12 acupuncture sessions at an acupuncturist’s clinic in the community. This study is the first randomized, controlled, double-blinded study on the efficiency of acupuncture treatment for depression, reported in the western scientific literature. However, 20 patients opted out themselves (they were not excluded by the study group) from the treatment before the completion of the 8-week intervention (13%). Random regression models of the intent-to-treat sample revealed that although patients receiving acupuncture improved better than those awaiting intervention, no evidence of differential efficacy of the depression-specific over the nonspecific intervention was found. Furthermore, the response rates in the acupuncture-treated patients were relatively low after 8 weeks (22% and 39% for specific and nonspecific intervention groups, respectively), with the response rate after the entire 16-week trial reaching 50%.
Occurrence—Worldwide; may be endemic and epidemic in debil- itated buy 1 mg anastrozole, malnourished or immunosuppressed infants discount anastrozole 1 mg amex. Pneumonitis in the compromised host may result from either a reactivation of latent infection or a newly acquired infection cheap anastrozole 1 mg fast delivery. Analysis of data from institutional outbreaks and animal studies indicates that the onset of disease often occurs 1–2 months after establishment of the immunosuppressed state. Susceptibility—Susceptibility is enhanced by prematurity, chronic debilitating illness and disease or treatments that impair immune mecha- nisms. Epidemic measures: Knowledge of the source and mode of transmission is so incomplete that there are no generally ac- cepted measures. Identiﬁcation—A subacute chlamydial pulmonary disease occur- ring in early infancy among infants whose mothers have chlamydial infection of the uterine cervix. Clinically, the disease is characterized by insidious onset, cough (characteristically staccato), lack of fever, patchy inﬁltrates on chest X-ray with hyperinﬂation, eosinophilia and elevated IgM and IgG. Many infants with pneumonia ultimately develop asthma or obstructive lung disease. Infectious agent—Chlamydia trachomatis of immunotypes D to K (excluding immunotypes that cause lymphogranuloma venereum). Occurrence—Probably coincides with the worldwide distribution of genital chlamydial infection. Mode of transmission—From the infected cervix to an infant during birth, with resultant nasopharyngeal infection (and occasionally chlamydial conjunctivitis). Control of patient, contacts and the immediate environment: 1) Report to local health authority: Ofﬁcial report not ordinarily justiﬁable, Class 5 (see Reporting). Identiﬁcation—An acute chlamydial respiratory disease with cough, frequently a sore throat and hoarseness, and fever at the onset; sputum is scanty and chest pain is rare. Radiographic abnormalities include bilateral inﬁltrates, sometimes with pleural effusions. Age distribution has 2 peaks: one in the pediatric population and one in those aged 60 or over. Outbreaks in community, household, daycare centers, and schools are often reported. Illness is usually mild, but recovery is slow, with cough persisting for 2–6 weeks; in older adults, bronchitis and sinusitis may become chronic. The organism can be isolated from throat swab specimens in the yolk sac of embryonated eggs, and cultured in special cell lines. Antibodies are rare in chil- dren under 5; prevalence increases among teenagers and young adults to a plateau of about 50% by age 20–30; prevalence remains high into old age. While clinical disease is encountered most frequently in young adults, disease has occurred in all age groups. No avian association has been found; no isolations or antibodies were found in pigeons and other birds captured at the site of an outbreak, nor in dogs or cats. Mode of transmission—Not deﬁned; possibilities include direct contact with secretions, spread via fomites and airborne spread. Period of communicability—Not deﬁned but presumably long; some military outbreaks have lasted as long as 8 months. Susceptibility—Presumably universal with increased likelihood of clinical disease in the presence of pre-existing chronic disease. Serological evidence of recall type immune response suggests immunity after infec- tion; second episodes of pneumonia have been observed in military recruits, with a secondary type of serological response to the second attack. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Obligatory report of epi- demics; no individual case report, Class 4 (see Reporting). The new macrolides, azithromycin and clarithromycin may also be used, as can the new ﬂuoroquinolones. Because these agents cause upper respiratory disease more often than pneumonia, they are presented under Respiratory Disease, Acute Viral. Pneu- monia is also caused by infection with rickettsiae (see Q fever) and Legionella (see Legionellosis). It can be associated with the invasive phase of nematode infections, such as ascariasis, and with mycoses such as aspergillosis, histoplasmosis and coccidioidomycosis. Various pathogenic bacteria commonly found in the mouth, nose and throat, such as Haemophilus inﬂuenzae, Staphylococcus aureus, Kleb- siella pneumoniae, Streptococcus pyogenes (group A hemolytic strepto- cocci), Neisseria meningitidis, Bacteroides species, Moraxella catarrha- lis and anaerobic cocci may produce pneumonia, especially in association with inﬂuenza, as superinfection following broad-spectrum antibio- therapy, as a complication of chronic pulmonary disease and after aspiration of gastric contents or tracheostomy. With increased use of antimicrobial and immunosuppressive treatment, pneumonias caused by enteric Gram-negative bacilli have become more common, especially those caused by Escherichia coli, Pseudomonas aeruginosa and Proteus species. Identiﬁcation—A viral infection most often recognized by the acute onset of ﬂaccid paralysis. Flaccid paralysis occurs in less than 1% of poliovirus infections; over 90% of infections are either inapparent or result in a nonspeciﬁc fever. A minor illness is recognized in 10% of infections with symptoms including fever, malaise, headache, nausea and vomiting. If the disease progresses to major illness, severe muscle pain and stiffness of the neck and back with ﬂaccid paralysis may occur. The paralysis of poliomyelitis is usually asymmetric, with fever present at the onset. The maximum extent of paralysis is reached in a short period, usually within 3–4 days. The site of paralysis depends on the location of nerve cell destruction in the spinal cord or brain stem. Some improvement in paralysis may occur during convales- cence, but paralysis still present after 60 days is likely to be permanent. Infrequently, recurrence of muscle weakness following recovery may occur many years after the original infection has resolved (“postpolio syndrome”); this is not believed to be related to persistence of the virus itself. Given the progress made towards global eradication, poliomyelitis must now be distinguished from other paralytic conditions by isolation of virus from stool. Other enteroviruses (notably types 70 and 71), echovi- ruses and coxsackieviruses can cause an illness simulating paralytic poliomyelitis. Differential diagnosis of acute nonparalytic poliomyelitis includes other forms of acute nonbacterial meningitis, purulent meningitis, brain abscess, tuberculous meningitis, leptospirosis, lymphocytic choriomeningitis, in- fectious mononucleosis, the encephalitides, neurosyphilis and toxic en- cephalopathies. Rises in antibody levels (4-fold or greater) are now less helpful in the diagnosis of wild poliomyelitis infection, since type-speciﬁc neutralizing antibodies may already be present when paralysis develops and signiﬁcant titre rises may not be demonstrable in paired sera. Furthermore, the antibody response following immunization mimics the response following infection with wild type viruses and the widespread use of live polio vaccines makes interpretation of antibody levels difﬁcult, although it may help in ruling out polio in cases where no antibody has developed in immunocompetent children. Infectious agent—Poliovirus (genus Enterovirus) types 1, 2 and 3; all types can cause paralysis. As a result of improved immunization worldwide and the global initiative to eradicate poliomyelitis, circulation of poliovi- ruses is limited to a decreasing number of countries. Poliomyelitis may be on the verge of worldwide eradication: only 7 countries remained endemic at end 2002 (Afghanistan, Egypt, India, Niger, Nigeria, Pakistan, Somalia). The greatest risks of polio are now on the Indian subcontinent (89% of cases in 2002) and in West Africa (10% of cases in 2002). Although wild poliovirus transmission has ceased in the majority of countries, importation remains a threat. A large outbreak of poliomyelitis occurred in 1992–1993 in the Netherlands among members of a religious group that refuse immunization. The virus was also found among members of a related religious group in Canada, although no cases occurred. Imported wild poliovirus has recently caused paralytic cases in countries as diverse as Algeria, Bulgaria, Burkina Faso, Georgia, Ghana, the Islamic Republic of Iran, Lebanon, Togo and Zambia. With the exception of rare imported cases, the few cases of poliomyelitis recognized in industrialized countries, until recent changes in immunization policy, were caused by vaccine virus strains. In tropical countries, a less pro- nounced seasonal peak occurred in the hot and rainy season. In the few remaining endemic countries, 80%–90% of cases are under 3 and virtually all cases are under 5. Clusters of susceptible persons, including groups that refuse immunization, minority populations, migrants and other unregistered children, nomads, refugees and urban poor are at high risk. Reservoir—Humans, most frequently people with inapparent infec- tions, especially children. Mode of transmission—Primarily person-to-person spread, princi- pally through the fecal-oral route; virus is detectable more easily and for a longer period in feces than in throat secretions.
Functional hyposplenism is associated with the following: hematologic diseases such as sickle cell hemoglobinopathies anastrozole 1mg low price, hemophilia; neoplasms such as chronic myeloid leukemia anastrozole 1mg without a prescription, non-Hodgkin’s lymphoma anastrozole 1 mg for sale, and following bone marrow transplantation; gastrointestinal disorders such as Crohn’s disease, ulcerative colitis, and Whipple’s disease, the degree of hyposplenism appears to be less in Crohn’s disease than ulcerative colitis; autoimmune disorders such as chronic active hepatitis, rheumatoid arthritis, Sjogren’s syndrome, and systemic lupus erythematosus; infiltrative diseases such as amyloidosis and sarcoidosis. Epidemiology The significance of postsplenectomy infections is in its excessive morbidity and mortality despite low incidence. The indications for splenectomy have been reevaluated and there is more conservative approach to splenic resection. Overall numbers are decreasing as well as the percentage of cases for particular indications. This has been the case primarily in two areas: splenic trauma and hematologic malignancies. The growing awareness of potential long-term complications continues to lead to more caution in the use of splenectomy with greater effort in surgery to preserve some splenic tissue (21–26). Microbiology Infections in asplenic or hyposplenic patients can occur with any organism, be it bacteria, virus, fungus, or protozoan. Acute and short-term complications in the perioperative period, such as subphrenic abscess, are high when multiple other procedures are performed. Delayed and long-term major risks include recurrent bacterial infections with encapsulated bacteria (10). Most cases (86%) occur in children younger than 15 years, but the overall incidence has decreased due to wide usage of conjugated H. Even though there is no conclusive evidence, many investigators feel that splenectomized patients are at high risk for fulminant meningococcemia (7). The organism is transmitted to humans by exposure to an animal, usually via bite or scratch, and can lead to fulminant sepsis (28). Infection in asplenic or hyposplenic settings can be associated with an eschar at the bite site and can produce intraleukocytic gram-negative bacilli in the Buffy coat or peripheral blood smear. Non-typhoid Salmonella species, which normally cause gastroenteritis, may cause disseminated infection in asplenic patients. Infections with gram-negative bacteria, notably Escherichia coli and Pseudomonas aeruginosa, also occur with increased frequency in splenectomized patients and are often associated with high mortality. Enterococcus species, Bacteroides species, Bartonella, Plesiomonas shigelloides, Eubacterium plautii, and P. Both Salmonella and Bartonella infection has been linked to reticuloendothelial blockade (32,33). Streptococcus suis,a zoonotic gram-positive bacteria, has been reported in several cases of bacteremias in asplenic individuals and is associated with swine exposure (34). Human granulocytic ehrlichiosis may be more severe, recurrent, with a prolonged course in individuals who are asplenic (35). Babesiosis caused by an intraerythrocytic protozoan, Babesia microti in North America and Babesia bovis in Europe has been reported to cause significant morbidity and mortality in asplenic hosts. In a review of 22 cases of babesiosis in splenectomized individuals, the infection was more severe and more likely associated with hemolytic anemia, high-grade and persistent parasitemia, and in some cases required exchange transfusion (36). In a recent study splenectomized patients secondary to trauma were twice as likely to have Plasmodium falciparum parasitemia and it was more likely to be associated with febrile symptoms. Mature parasites were seen more often in the peripheral blood in asplenic individuals (37). Severe Infections in Asplenic Patients in Critical Care 353 A high index of clinical suspicion must be maintained for febrile presentations in the asplenic patient or one with a chronic disease that can produce a dysfunctional spleen. Patients may present with nonspecific symptoms like, low-grade fever, chills, rigors, pharyngitis, muscle aches, and vomiting and diarrhea that might have been present for one to two days prior to clinical deterioration (10). In the setting of known asplenia or splenic dysfunction any febrile illness with or without focal symptoms must be suspected to be postsplenectomy sepsis. In children younger than five years, however focal infections, particularly meningitis are more prominent. Bacteria can be seen on microscopic examination of peripheral blood and in multiple organ systems in autopsied cases (40–44). Other sequelae include, deafness associated with meningitis and mastoid osteomyelitis, and aortic insufficiency following endocarditis (45,46). Bacteria can be visualized on Gram stain or Wright stain of the peripheral blood Buffy coat, and if seen on peripheral blood 6 smear it suggests a quantitative bacteremia of >10 /mL, which is four logs or greater than that of usual bacteremia. Because of this degree of bacteremia, blood cultures are positive in 12 to 24 hours. Standard lab tests like complete blood count, serum chemistries, and appropriate radiologic studies should be done. Further tests, including the peripheral smear for malaria or babesiosis, should be guided by the patient’s history. Furthermore, Howell–Jolly bodies or other evidence of hyposplenism should be sought, especially in an individual with a history of an illness predisposing to hyposplenism. However, the literature does support that an aggressive approach improves survival (48). Despite the absence of any controlled studies, self- administration of an antibiotic at first sign of suspicious illness in the asplenic or hyposplenic person is advised, this should be specially instituted if delivery of medical care is not immediately available. In an outpatient setting, a patient suspected to have postsplenectomy sepsis should receive an appropriate broad-spectrum antimicrobial such as ceftriaxone parenterally prior to hospital transfer, whether or not blood cultures are obtained. Local resistance patterns should be taken into account when selecting an initial presumptive regimen, with consideration of antibiotic, such as ceftriaxone and cefotaxime, which are active against penicillin-resistant pneumococci, as well as beta-lactamase producers such as H. Some penicillin-resistant pneumococcal isolates are also resistant or only intermediately susceptible to cephalosporins. If such resistance is suspected, the use of vancomycin combined with gram-negative antibiotic coverage for organisms such as meningococcus must be considered. High-level penicillin-resistant pneumococci will definitely require vancomycin with or without rifampin. Other choices include an anti-pneumococcal quinolone, such as levofloxacin, amoxicillin/clavulanic acid, trimethoprim/sulfamethoxazole, or a newer macrolide (clarithromycin, azithromycin). The decision to broaden the gram- negative coverage to other gram negatives including P. In patients with known or suspected central nervous system infections, vancomycin with or without rifampin plus a third-generation cephalosporin is the most optimal initial therapy. Intravenous immunoglobulin is another intervention that has been shown to decrease mortality in asplenic animals (49,50). Granulocyte-macrophage colony– stimulating factor has increased macrophage bactericidal activity in eusplenic and asplenic mice. Babesiosis in the asplenic host is best treated with a combination of clindamycin and quinine. Exchange transfusions to lower high levels of parasitemia also have been used (52,53). Other therapeutic modalities, such as vasopressors, may be warranted in selected cases. Prevention Preventive strategies fall into three major categories: education, immunoprophylaxis, and chemoprophylaxis (33,54). Most patients with asplenia (11% to 50%) remain unaware of their increased risk of serious infection or the appropriate health precautions that should be undertaken (55,56). Asplenic patients should be encouraged to wear a Medi-Alert bracelet or necklace and carry a wallet explaining their lack of spleen and other medical details (33). Patients should be explained regarding the potential seriousness of postsplenectomy sepsis and rapid time course of progression. Patients should be instructed to notify their physician in the event of any acute febrile illness and proceed to nearest emergency department. They should inform any new health care provider, including their dentist, of their asplenic or hyposplenic status. Patients should also be educated regarding travel-related infections such as malaria and babesiosis. Malaria chemoprophylaxis relevant to the local pattern of infestation should be prescribed and preventive measures implemented to reduce mosquito bites (33,54). They should also be educated regarding prompt treatment of even minor dog or other animal bites. Asplenia or hyposplenism itself is not a contradiction for routine immunization including live vaccines. Vaccination significantly reduces the risk of bacteremia of any cause beyond the postoperative period, and vaccinated patients carry a lower risk of infection than non-vaccinated ones (57).
Period of communicability—Variable; may extend intermittently over several years when moist lesions are present buy 1 mg anastrozole free shipping. Infec- tion results in immunity to reinfection and may offer some protection against infection by other pathogenic treponemes order 1 mg anastrozole fast delivery. Preventive measures: The following apply to yaws and other nonvenereal treponematoses generic anastrozole 1mg otc. Although present techniques can- not differentiate the infectious agents, differences observed among clinical syndromes are unlikely to result from epidemio- logical or environmental factors alone. Periodic clinical resurveys and continuous surveillance are essential for success. Differentiation of venereal and nonvenereal treponema- toses, with proper reporting of each, has particular impor- tance in the evaluation and consolidation of mass campaigns. In low-prevalence areas, treat all active cases, all children and close contacts of infectious cases. For patients 10 years or older with active disease and contacts, a single injection of benza- thine penicillin G, 1. Essential features are: 1) examining a high percentage of the population through ﬁeld surveys; 2) extending treatment of active cases to family and community contacts based on the demonstrated prevalence of active yaws; 3) surveys at yearly intervals for 1–3 years, as part of the established rural public health activities of the country. Disaster implications: None observed, but potentially a risk in refugee or displaced populations in endemic areas without hygienic facilities. International measures: To protect countries against risk of reinfection where active mass treatment programs are in progress, adjacent countries in the endemic area should institute suitable measures against yaws. Movement of infected people across frontiers may require supervision (see Syphilis, section I, 9E). Identiﬁcation—Acute infectious viral disease of short duration and varying severity. The mildest cases may be clinically indeterminate; typical attacks are characterized by sudden onset, fever, chills, headache, back- ache, generalized muscle pain, prostration, nausea and vomiting. The pulse may be slow and weak out of proportion to the elevated tempera- ture (Faget sign). Some cases progress after a brief remission of hours to a day into the ominous stage of intoxication manifested by hemorrhagic symptoms including epistaxis, gingival bleeding, hemateme- sis (coffee-ground or black), melaena, and liver and renal failure; 20%–50% of jaundiced cases are fatal. The overall case-fatality rate among indigenous populations in endemic regions is 5% but may reach 20%–40% in individual outbreaks. Serological diagnosis includes demonstrating speciﬁc IgM in early sera or a rise in titre of speciﬁc antibodies in paired acute and convalescent sera. Recent infections can often be distinguished from vaccine immunity by comple- ment ﬁxation testing. Infectious agent—The virus of yellow fever, of the genus Flavivirus and family Flaviviridae. Occurrence—Yellow fever exists in nature in 2 transmission cycles, a sylvatic or jungle cycle that involves Aedes or Haemagogus mosquitoes and nonhuman primates, and an urban cycle involving humans and mainly Aedes aegypti mosquitoes. Sylvatic transmission is restricted to tropical regions of Africa and Latin America, where a few hundred cases occur annually, most often among occupationally exposed young adult males in forested or transitional areas of Bolivia, Brazil, Colombia, Ecuador and Peru (70%–90% of cases reported from Bolivia and Peru). Historically, urban yellow fever occurred in many cities of the Americas; no outbreak of urban yellow fever has occurred for 50 years in North America. There is no evidence that yellow fever has ever been present in Asia; in western Kenya, sylvatic yellow fever was reported in 1992–1993. Reservoir—In urban areas, humans and Aedes mosquitoes; in forest areas, vertebrates other than humans, mainly monkeys and possibly marsupials, and forest mosquitoes. Transovarian transmission in mosqui- toes may contribute to maintenance of infection. Humans have no essential role in transmission of jungle yellow fever, but are the primary amplifying host in the urban cycle. Mode of transmission—In urban and certain rural areas, the bite of infective Aedes mosquitoes. In South American forests, the bite of several species of forest mosquitoes of the genus Haemagogus. Period of communicability—Blood of patients is infective for mosquitoes shortly before onset of fever and for the ﬁrst 3–5 days of illness. The disease is highly communicable where many susceptible people and abundant vector mosquitoes coexist; it is not communicable through contact or common vehicles. Susceptibility—Recovery from yellow fever is followed by lasting immunity; second attacks are unknown. Transient passive immunity in infants born to immune mothers may persist for up to 6 months. Preventive measures: 1) Institute a program for active immunization of all people 9 months or older who are exposed to infection because of residence, occupation or travel. Antibodies appear 7–10 days after immunization and may persist for at least 30–35 years, probably much longer, though immunization or reim- munization within 10 years is required by the International Health Regulations for travel from endemic areas. The vaccine can be given any time after 6 months of age and can be administered with other antigens such as measles vaccine. The vaccine is contraindicated in the ﬁrst 4 months of life and should be considered for those aged 4–9 months only if the risk of exposure is judged to exceed the risk of vaccine-associated encephalitis, the main complication in this age group. The vaccine is not recommended in the ﬁrst trimester of pregnancy unless the risk of disease is believed to be higher than the theoretical risk to the pregnancy. There is no evidence of fetal damage from the vaccine, but lower rates of maternal seroconversion have been observed, an indication for reimmunization after delivery or termina- tion. Protective clothing, bednets and repellents are ad- vised for those not immunized. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Case report universally required by International Health Regulations; Class 1 (see Reporting). Prevent access of mosquitoes to patient for at least 5 days after onset by screening the sickroom, by spraying quarters with residual insecticide, and by using insecticide-treated bednets. Search patient’s premises and places of work or visits over the preceding several days for mosquitoes capable of transmitting infec- tion; apply effective insecticide. Investigate mild febrile illnesses and unexplained deaths suggesting yellow fever. Conﬁrmation by the histopathological examination of livers of moribund or recently dead monkeys or by virus isolation is highly desirable. Serological surveys of human populations are not useful where yellow fever vaccine has been widely used. Disaster implications: Mass vaccination may be considered if an epidemic is feared. The International Certiﬁcate of Vaccination against Yellow Fever is valid for 10 years from 10 days after date of immunization; if reimmunization occurs within that period, valid 10 years from date of reimmunization. Identiﬁcation—Infection caused by enteropathogenic Yersinia typically manifested by acute febrile diarrhea with abdominal pain (espe- cially in young children). Other clinical manifestations (extraintestinal or otherwise) include acute mesenteric lymphadenitis mimicking appendici- tis (especially in older children and adults) and systemic infections. The most common post-infectious complications are erythema nodosum (about 10% of adults, particularly women), and reactive arthritis. Bloody diarrhea occurs in up to one-fourth of patients with Yersinia enteritis; diarrhea may be absent in up to a third of Y. The organisms may be recovered on usual enteric media if precautions are taken to prevent overgrowth of fecal ﬂora. Cold enrichment in buffered saline at 4°C (39°F) for 2–3 weeks can be used but this procedure usually enhances the isolation of non-pathogenic species. Strains pathogenic for humans are those of biotypes 1B, 2, 3 and 4; they are pyrazinamidase- negative. Biotype 1A strains are non-pathogenic whereas the very rare strains of biotype 5 have been isolated from hares. Human cases have been reported in association with disease in household pets, particularly puppies and kittens. The highest isolation rates have been reported during the cold season in temperate climates, including northern Europe (especially Scandinavia), North America and temperate regions of South America. Contamination through milk (including pasteurized milk, where postpasteurization contamination is more likely than resistance of the agent to the pasteurization process) is less common.
Richmond Rascals. 12 Richmond Hill. Richmond-Upon-Thames. TW10 6QX tel: 020 8948 2250