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Recovery of visual acuity in cases with optic neuritis was a prominent clinical result (Dorst, 2016; Koziolek, 2012). Early initiation of therapy, within 14-20 days of onset of symptoms, is a predictor of response. Evidence-based guideline update: plasmapheresis in neurologic disorders: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Immunoadsorption with regenerating columns in treatment of steroid refractory relapse in multiple sclerosis and optic neuritis. Response to therapeutic plasma exchange as a rescue treatment in clinically isolated syndromes and acute worsening of multiple sclerosis: a retrospective analysis of 90 patients. Immunoadsorption in steroid-refractory multiple sclerosis: clinical experience in 60 patients. Tryptophan immunoadsorption during pregnancy and breastfeeding in patients with acute relapse of multiple sclerosis and neuromyelitis optica. Therapeutic apheresis in multiple sclerosis and other central nervous system disorders. Immunoadsorption therapy in patients with multiple sclerosis with steroid-refractory optical neuritis. Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demylination. Basic and escalating immunomodulatory treatments in multiple sclerosis: current therapeutic recommendations. Comprehensive systematic review summary: disease-modifying therapies for adults with multiple sclerosis. Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Escalation therapy of steroid refractory multiple sclerosis relapse with tryptophan immunoadsorption - observational multicenter study with 147 patients. Differences in the response to apheresis therapy of patients with 3 histopathologically classified immunopathological patterns of multiple sclerosis. Meta-analysis of clinical studies of the efficacy of plasma exchange in the treatment of chronic progressive multiple sclerosis. A randomized trial of plasma exchange in acute central nervous system inflammatory demyelinating disease. The antibodies induce weakness of skeletal muscles, which can be generalized or localized, and nearly always includes eye muscles causing diplopia and ptosis. Antibodies against titin, agrin, and ryanodine receptor may be suggestive of more severe disease. In antibody-negative cases (10-15%), neurophysiological tests and a characteristic response to therapy secure the diagnosis. Cholinergic side effects, including diarrhea, abdominal cramping, increased salivation, sweating and bradycardia, are dose limiting.

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This increased response time is thought to result from inhibitory processes acting upon the distracting stimulus during the prime trial, to prevent further processing. Older adults show a similar increase in processing time as compared to younger adults. Thus, we can infer that inhibitory deficits are not always present in the older adult population. As with the processing speed account, the inhibitory deficit hypothesis may not describe all of the cognitive changes that accompany aging because it does not posit an environmental support mechanism. This mechanism, proposed by Craik and Byrd [74], suggests that older adult performance can improve if support and encoding and/or retrieval are instantiated. That improvement suggests an interaction between working memory and episodic long-term memory. That interaction, along with the changes in other cognitive domains and increases in cognitive variability suggest that theories of cognitive aging need to more broadly focus on the interaction between changes in the prefrontal cortex (associated with working memory and executive function) and changes in the hippocampus (associated with episodic memory). Research over the last 30 years has painted a rather complex picture of cognitive aging. We gerontologists now are beginning to understand the important relationship between changes in the brain associated with normal aging and the resulting behavioral manifestations. We must consider an interdisciplinary approach in order to further our understanding of normal cognitive aging. Interdisciplinary research is scientifically necessary to the understanding of the complexity of the global phenomenon of cognitive aging. Thus, it is necessary to put, for example, biomedical researchers and social researchers in dialogue. This emerging knowledge can elucidate the global picture of the complexity of aging. This chapter attempts an interdisciplinary look at cognitive aging through the shared lens of clinical and cognitive psychologists. Through that lens we better understand the weaknesses and holes in our present conceptualization of cognitive aging. Through that lens we can also now begin to develop a perhaps more useful meta-theory to facilitate bridge-building between diverse theories produced in the scientific space of cognitive aging. Regional brain changes in aging healthy adults: general trends, individual differences and modifiers. Meta-analyses of agecognition relations in adulthood: estimates of linear and nonlinear age effects and structural models. Aging associations: influence of speed on adult age differences in associative learning. Age related, regional, hemispheric, and medial-lateral differences in myelin integrity in vivo in the normal adult brain. Aging and myelinated nerve fibers in prefrontal cortex and corpus callosum of the monkey.

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Therefore, the findings provided for each of the sections reflect the variability of the data. One patient with bilateral cochlear nerve deficiency also had unilateral vestibular nerve deficiency. Sixteen of 18 patients had cochlear dysplasia (bilateral in 7) with most patients (n 7) having 1. Olfactory Apparatus and Face Only 2 patients of 10 had choanal atresia (Fig 4), and 1 of those 2 had a deficient posterior nasal septum. A percentage was chosen as the representation because some findings were bilateral and others were singular, and some of the structures could not be evaluated in all patients due to differences in imaging technique. Inner ear dysplasia, olfactory structure hypoplasia, and skull base hypoplasia were the most frequent findings. Four additional patients had hypoplastic parotid glands bilaterally (2 of which had accessory salivary tissue along the masseter). The other 9 patients had basioccipital hypoplasia, none of which had classic basilar invagination. All 10 patients had a normal relationship of the superior ossification center of the dens with respect to the anterior arch of C1. However, 7 of 10 demonstrated a dorsally angled clivus, with posterior displacement of an ossific density, which we interpreted to reflect an underdeveloped basioccipital ossification center and widening of the spheno-occipital synchondrosis (Fig 9). Eight of 10 had hypoplasia of the sella with 7 of those patients having a "J-shaped" appearance, with flattening and elongation of the tuberculum sella (Fig 9B). Two of 10 patients demonstrated aplastic Venous Anomalies In 2 of the 10 patients, the readers reported insufficient imaging data to accurately assess the venous structures. Of the remaining 8 patients, 6 demonstrated large anomalous transmastoid emissary veins (Fig 10), with 3 of these patients demonstrating this finding bilaterally. In 5 of the 6 patients with anomalous transmastoid emissary veins, the ipsilateral sigmoid sinus was hypoplastic. Inner ear abnormalities were the most frequent finding, whereas coloboma and choanal atresia were infrequent findings. There is also the suggestion of left inferior vestibular nerve hypoplasia (arrow). The first is olfactory complex anomalies, which include either absence or hypoplasia of the olfactory nerve, sulcus, and bony groove. Our series demonstrated 9 of 10 patients with basioccipital hypoplasia, similar to the work of Fujita et al. This of the patients with bilateral transmastoid emissary veins also finding has not been previously reported. The spheno-occipital demonstrated bilateral enlarged transoccipital emissary veins. We suspect that the posteriorly displaced basioccipital ossification center can Central Nervous System mimic basilar invagination.

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The majority of cancers were isolated types, but there was a cluster of breast cancer cases. In describing the malignancy risk in the controlled trials, is it appropriate to consider all diagnosed cancers, regardless of cell type, or should the assessment focus only on the cluster of breast cases? This should include all documented cases of malignancy in any patient who received ocrelizumab, regardless of whether the drug was received on a controlled trial or not, and regardless of whether the treatment was received during the randomized or open-label portion of the trial. Considering the low number of events and limited follow up cited by Genentech, do you view the imbalance in breast cancer diagnoses (6 vs. The narratives for each of the above cases were reviewed and assessed for details, including age of the patient at cancer diagnosis, number of days on therapy with ocrelizumab, presence of family history of breast or other cancers, and pertinent pathological tumor characteristics and stage at diagnosis. Although it is difficult to make any conclusions about whether there is cause for concern, with respect to the imbalance in cases diagnosed in ocrelizumab treated patients, a potential safety signal should not be ruled out, at this time. If you agree with Genentech that no conclusion on malignancy can be made, do you think it is appropriate to further evaluate this signal in the post-marketing period as proposed? The signal identified within the trials in the ocrelizumab does warrant further evaluation, and should include collection of information on newly diagnosed malignancies, in general. Specific guidance should be given to the Sponsor on the information collected going forward, but should include, at a minimum, the pathological cancer diagnosis, stage at diagnosis, time on therapy with ocrelizumab at the time of cancer diagnosis, and action taken with ocrelizumab therapy at that point (continue vs. Although it is difficult to make a conclusion about whether causality can be attributed to ocrelizumab in any of the cancer cases identified, a relationship should not be ruled out, at this time. We think that there is precedent for including the information about potential malignancy risk in the product labeling. For example, other products such as olaparib (Lynparza) and alemtuzumab (Lemtrada) include information on cases of malignancy in the label and have malignancy risk as a section in Warnings and Precautions. Using these examples, it is warranted to have further discussions with the Sponsor regarding the need to include this information in the label. Narrative states she had breast biopsy D451 with malignant cells and had R mastectomy D471. According to the narrative, on study day 737 she had U/S L breast which revelaed hypogenic tumor. She had radical mastectomy, but diagnosis was deemed unrelated to study drug by investigator. On study day 917, patient had a R breast biopsy, which revealed infiltrating ductal carcinoma. Narrative states that patient had h/o bilateral breast fibroaednomas treated with partial breast resection in 2005.

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Parasitology 90 Pneumocystis carnii Geographical Distribution: world wide Habitat:-In the interstitial plasma cells of the lung (alveoli, epithelial cells) of man and other animals Morphology:-Trophozoite Foam-like mass in the lung Amoeboid form Has single nucleus Cyst:size: 4-5m in diameter Shape: spherical Contents eight comma shaped sporozoites Resembles a fungus Life Cycle:-The complete life cycle of this parasite is unknown. Previously it was regarded as a non-pathogenic yeast; however, more recent studies confirm its identity as a sporozoan and place it in the family sporozoa. It should be borne in mind when causes of intestinal disorder are sought, esoecially in the absence of other identified causes of diarrhea or gastrointestinal symptoms should be assessed for the presence of B. It is found in stool specimens obtained from asymptomatic individuals as well as those with persistent diarrhea. It may also be detected in wet mounts or trichromestained smears of faecal specimen. It has a peripheral cytoplasm, a central vacuole but no nucleus Relevance to Ethiopia There is only a few recent studies which determined the prevalence of B. A, two cases among the 190 patients were detected (Fisseha B et al, Ethiop J Health Dev. In many endemic areas it is becoming increasingly difficult to control because of Anopheline mosquito vector and the parasite to develope resistance to various eradication and treatment options. Infective stage to man from the insect vector is sporozoites and to the insect vector from man is gametocytes. Geographical Distribution Malaria is endemic in 91 countries with about 40% of the world population is at risk. Plasmodium falciparum is the most prevalent species in the hotter and more humid regions of the world. Unlike the other species, it is more common and well adapted to the temperate region than in the tropics. Infection rates in Ethiopia are about 60%, Parasitology 94 40%, 1% and less than 1% for P. Habitat: the parasite enters the blood and carried to the parenchyma cells of liver, where they multiply enormously. Morphology There are sequential developmental stages with distinct morphological features that helps for species identification in Romanowsky stains of Peripheral blood films. Often contain several parasites Density: often high density of parasites Plasmodium Vivax Rarely more that 2% of cells infected Young Trophozoites Size; 0. Infected Red Blood Cells Youngest erythrocytes are infected Parasite Density: medium Plasmodium Malariae Young Trophozoite Size: Up to 1/3 Red blood cell. Rarely more than 2% of cells infected About 20-30% of cells may become oval with fimbriated ( ragged ) ends General Life Cycle of Malaria parasites: -Malaria parasites require two hosts to complete their life cycle. Female Anopheles mosquitoes as the definitive host, where sexual reproduction (sporogony) takes place and human being as the intermediate host, where the asexual reproduction (schizogony) takes place. Sporozoites from infected female Anopheles mosquito are injected with the saliva into the blood circulation of man when the vector takes a blood meal.

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Anxiety: Anxiety is also a frequent psychiatric disorder associated with cancer [68]. Significant levels of anxiety were reported by 32% of the patients [74], which exceeds levels reported in the general population; in contrast, depression was reported by 12% of the sample. In fact, 80% of the patients with tumors in the right cortex or left cerebellum reported elevated anxiety symptoms. The association of anxiety and tumor loci was not confounded by demographic, 3 Neuropsychological Problems in Neuro-oncology 45 disease, or treatment variables. Results evidenced the risk that neuro-oncology patients face for developing significant anxiety symptoms that may not rise to the awareness of parents or the treatment team. Making a correspondence between the autistic-like behaviors and the brain tumor is not trivial. Clinical observations suggest that children with those behaviors, that is, with (1) abnormalities in social cognition or social behaviors, (2) distress when environmental structure or schedule is altered, (3) hyperfocus on limited personal interests, and (4) stereotypical body or speech expressions, often have lesions in the cerebellar hemispheres and/or the temporal lobes. The cerebellum and temporal lobes have been the regions most closely associated with autism (see Chapter 10 by Dr. For individuals with brain tumors, secondary neurobehavioral diagnoses should make clear that the terms are used descriptively and that the full syndrome may not be present. Cognitive affective syndrome: the cognitive affective syndrome, defined by significant deficits in executive function (planning and set shifting), spatial cognition, language (nonmotor expressive), abstract reasoning, attentional regulation, memory, and personality (hyperactivity, impulsivity, disinhibition, and emotional lability), is associated with bilateral or large unilateral lesions in the posterior cerebellar lobes, vermis, and in pan cerebellar disorders [77]. It was first described by Schmahmann and Sherman in 1997 [78] and is often associated with cerebellar mutism. While other neurological disorders and even congenital cerebellar disorders can also cause this disorder [84], such behavioral abnormalities can be difficult to understand in someone who has a tumor in the cerebellum. The co-occurrence of the cognitive and affective symptoms is thought to arise from the disruption of the cerebello-thalamo-cortical and cortical-pontine-cerebellar tracts connecting the cerebellum with frontal, parietal, temporal, and limbic cortices. There are no known medications that address the symptoms of the cognitive affective syndrome. However, behavioral techniques applied from the field of autism can be helpful, along with careful construction of daily routines and sleep hygiene habits. Of course, the etiology is neurological 2 Cerebellar mutism is an acquired complete loss of speech, transient in nature, most often following surgical resection of cerebellar or intrinsic posterior fossa tumors or following stroke or trauma. Hypothalamic syndromes: Tumors originating in the hypothalamus are, first, associated with disorders of eating behavior, often causing hyperphagia, and with symptoms similar to anorexia [86] that are actually loss of appetite, or even cachexia. However, they produce other symptoms that lead to changes in growth rate and to hyperactivity, irritability, attacks of anxiety, euphoria, aggressiveness, disruptions of vision, sleep disturbance, and headaches. Gelastic seizures (inappropriate episodes of smiling, giggling, or laughter that are accompanied by electroencephalographic changes) are a rare hypothalamic phenomenon.

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Thinking on your feet: a neuropsychological review of peripheral vascular disease. Neurologic and neuropsychological morbidity following major surgery: comparison of coronary artery bypass and peripheral vascular surgery. Carotid surgery, cognitive function, and cerebral blood flow in patients with transient ischemic attacks. The mind of a failing heart: a systematic review of the association between congestive heart failure and cognitive functioning. Cognitive functioning and chronic heart failure: a review of the literature (2002-July 2007). Cognitive dysfunction as a major determinant of disability in patients with heart failure: results from a multicentre survey. The effects of cognitive impairment on mortality among hospitalized patients with heart failure. Neuropsychological function in patients with end-stage heart failure before and after cardiac transplantation. Cyclosporine may affect improvement of cognitive brain function after successful cardiac transplantation. Hypotension and cognitive impairment: selective association in patients with heart failure. Smith, Juliana Sanchez Bloom, and Nancy Minniti Introduction Brain injury due to cerebrovascular disease is a common cause of cognitive dysfunction in adults and a clinically significant cause of disability in children. Stroke, defined as brain injury due to a disruption of cerebral blood flow, has an incidence of 94/100,000 age-adjusted person-years in high income countries and 117/100,000 age-adjusted person-years in lowmiddle income countries [1]. As many as 65% of adults experience new or worsening cognitive deficits following stroke [2], and in one small series of children with stroke, 75% had persistent cognitive deficits [3]. Therefore, assessment of neuropsychological function following stroke is an important part of the medical management of these patients. Less commonly, a blood clot develops within one or more veins that drain the brain, known as cerebral venous sinus thrombosis, and leads to venous infarction. Risk Factors for Cerebrovascular Disorders In adults, arterial ischemic stroke is commonly associated with advancing age, hypertension, atrial fibrillation, smoking, and diabetes mellitus [4]. Other risk factors include obesity, cardiac disease, carotid stenosis, sickle cell anemia, recent infection, and alcohol abuse. In young adults abnormalities of blood vessel structure such as arterial dissection, non-inflammatory vasculopathies, and vasculitis are also associated with stroke [5]. In addition, hematologic abnormalities leading to hypercoagulability may play a role in selected cases [6]. Cerebral venous sinus thrombosis, which can result in either ischemic or hemorrhagic infarction, is associated with oral contraceptive use; infections of the head, neck, or central nervous system; malignancy; prothrombotic states; inflammation; and pregnancy [7].

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Secondary therapies include cyclosporine, interferon, azathioprine, and cyclophosphamide, and other immunosuppressive therapies. Allo- or autoantibodies bind to coagulation factor and cause clearance by reticuloendothelial system or inhibit their functions, both of which result in bleeding tendency. Current management/treatment In patients with factor inhibitors, the therapy should be individualized, depending on the clinical setting, presence or absence of bleeding, and the inhibitor titer. The goals of therapy include cessation of bleeding and suppression of inhibitor production. Rationale for therapeutic apheresis For patients with inhibitor the extracorporeal removal of antibodies with immunoadsorption is more effective than plasma exchange. These effects include a decrease in activated monocytes and cytotoxic T cells, a change in T cell population, and a decrease in autoreactive T cell activity. Immunosorba1 utilizes two columns; one regenerates immunoglobulins while the other is adsorbing them. Post-procedure antibody titer may be elevated due to the re-equilibration of antibodies from extravascular to intravascular space. Hypoprothrombinemia associated with lupus anticoagulant is treated with prothrombin complex concentrate and corticosteroids. Technical notes To remove inhibitors, plasma flow rates are 35-40 mL/minute in Immunosorba1; a three plasma-volume treatment (10 L) requires 20-30 adsorption cycles. The aggregates of cryoglobulins can deposit on small vessels and cause damage by activating complement and recruiting leukocytes. This most likely occurs on the skin of lower extremities because of exposure to lower temperatures. The end-organ complications secondary to cryoglobulinemia range from none to severe. Cryoglobulinemia is associated with a wide variety of diseases including lymphoproliferative disorders, autoimmune disorders, and viral infections. The diagnosis of cryoglobulinemia is made by history, physical findings, low complement levels and detection and characterization of cryoglobulins (cryocrit). Additionally, interferon and ribavirin are used for the treatment of cryoglobulinemia related to hepatitis C infection. It is used in all types of cryoglobulinemia for a wide variety of clinical manifestations. Double cascade filtration, which separates plasma out of whole blood in the first filter and removes high molecular weight proteins in the second filter (such as IgM), has also been used to treat cryoglobulinemia. Another apheresis modality used in this disease is cryofiltration or cryoglobulinapheresis, which cools the plasma in an extracorporeal circuit either continuously or in a 2 step procedure to remove cryoglobulins, the remaining plasma is warmed to body temperature prior to returning to the patient.

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Mansonella Perstans Geographical Distribution Widely distributed in South America and tropical Africa. Habitat Adults: In the serous cavities, mesentery, and connective tissue, especially the retroperitoneal. Microfilariae: In peripheral blood at any time because non-periodic guts mouth parts. They commonly migrate rapidly in the body and may be seen in the subconjunctival tissue of the eye or in thin skinned areas. Morphology: Adults; Male: about 40mm Female: 7 cm - 8 cm Microfilariae Size: 190-240 m long by 4. Life Cycle Man is the definative host and female culicoides are the intermediate hosts. Avoid the bite of vectors Destruction of insect vectors Treatment and health education. Laboratory Diagnosis Finding the characteristic microfilaria in the stained blood films at any time. Habitat Adults: In the mesentery, retroperitoneal tissue, abdominal wall, and lymphatic vessels of man. Infective larvae: In the gut, and mouth parts of culicoides and simulium black flies Parasitology 213 Morphology: Adults:-Male: about 35mm -Female: 70mm Microfilariae:-Size: 150-200 m long and 4. Life cycle Man is the definitive host and the infective larvae are transmitted by the bite of culicoides and simulium species as an intermediate hosts. Most infections are asymptomatic or cause chronic arthritis, skin rashes and other symptoms. Laboratory Diagnosis Finding the microfilariae in stained blood film and occasionally in skin snip at any time since it is nonperiodic. Mansonella Streptocerca Geographical Distribution:- Found only in the rain forest of Africa especially in Ghana, Nigeria, Zaire and Cameroon. Habitat Adults: In cutaneous connective tissues of the chimpanzee, Parasitology 214 Microfilariae: In the skin of man by day and by night, but are not found in the blood Infective larvae: In the gut, muscle tissue and mouth parts of Culicoides midges. Morphology Adults: are recovered only in animal hosts and in man only microfilariae is known. Life cycle Like other filarial worms It requires two hosts to complete its life cycle man as a definitive host and culicoides as its intermediate host. Most infections are asymptomatic or sometimes cause an itching dermatitis, hypopigmented macules and thickening of the skin.

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A third class of laxatives has mainly stimulating (propulsive) effects on the intestinal wall, causing inhibition of the reabsorption of fluids in the colon and increasing the secretion of fluids and electrolytes into the intraluminal cavity. Therefore, always listen to the patient and change therapy according to the needs of your patient. Using selective opioid antagonists to block the intestinal side effects of opioids would be an "intelligent" approach to constipation therapy in patients with an Abdominal Cancer, Constipation, and Anorexia indication for permanent or long-term opioid therapy. In fact, this approach is based on an interesting hepatic mechanism: morphine is metabolized in the liver into its active products, while the opioid antagonist naloxone is completely metabolized in its first pass through the liver into inactive forms. Therefore, the antagonist would only be active at the intestinal opioid receptors, specifically antagonizing the constipation side effects of morphine or other opioids. Due to its route of application and high costs, its use is limited to "emergency situations," when intestinal paralysis, not merely obstruction, is imminent. Patients must be educated about the fact that the cancer induces certain changes in the central regulation of appetite. When initial pain readings are high, intravenous titration of morphine may be used to estimate the (additional) daily opioid requirements of the patient (this only applies to cancer patients! Always educate patients about the constipating effects of opioids and advise them to take laxatives. Myeloma is the hematological malignancy most frequently associated with lytic bone lesions. Bone metastases are more often seen with cancer of the lung and the prostate in males and cancer of the breast in females; up to 85% of patients dying from breast, prostate, or lung cancer demonstrate bone involvement at autopsy. The most common cancer that produces pain metastasis is breast cancer, and the most common site is vertebral bodies, as seen in Table 2. The resulting sclerotic metastases are less prone to fracture because of the locally increased bony mass. Osteoclasts can be activated by tumor products or indirectly through an influence on other cells. Tumor cells frequently produce factors that can activate immune cells, which release powerful osteoclast-stimulating substances, such as tumor necrosis factor and interleukins 1 and 6. Osteoclastic activity leads to collagen fragments such as pyridinoline and deoxypyridinoline that can be measured in urine. While about 80% of patients with breast cancer will develop osteolytic or osteoblastic metastases, about Table 3 Characteristics of skeletal assessment in the most common tumors associated with bone metastases Myeloma Hypercalcemia Bone scans Alkaline phosphatase Histology X-ray 30% Osteoclastic Osteolytic Breast 30% + + Mixed Mixed Prostate Rare ++ ++ Osteoblastic Sclerotic Osseous Metastasis with Incident Pain two-thirds of all demonstrated sites of bone metastases are painless. Microfractures occur in bony trabeculae at the site of metastases, resulting in bone distortion.

References:

  • https://dchealth.dc.gov/sites/default/files/dc/sites/doh/publication/attachments/Pneumonia%20fact%20sheet.pdf
  • https://www.doh.wa.gov/Portals/1/Documents/Mtgs/2018/CHWConference/MensHealth-PAPA.pdf
  • http://211.76.170.15/server/APJCN/24/3/387.pdf
  • http://webs.fcm.unc.edu.ar/wp-content/blogs.dir/30/files/2018/03/Fever-of-Unknown-Origin-A-Clinical-Approach.pdf