Dengue haemorrhagic fever This is a more severe form of the disease which usually occurs in young children; it is largely con?ned to the indigenous population(s) of south-east Asia. It is accompanied by signi?cant complications and mortality. Immunological status of the host is considered important in pathogenesis.... dengue
Persistent heartburn may be a sign of more serious oesophageal disease and medical advice should be sought.... heartburn
Visceral leishmaniasis (kala-azar) A systemic infection caused by Leishmania donovani which occurs in tropical and subtropical Africa, Asia, the Mediterranean littoral (and some islands), and in tropical South America. Onset is frequently insidious; incubation period is 2–6 months. Enlargement of spleen and liver may be gross; fever, anaemia, and generalised lymphadenopathy are usually present. Diagnosis is usually made from a bone-marrow specimen, splenic-aspirate, or liver-biopsy specimen; amastigotes (Leishman-Donovan bodies) of L. donovani can be visualised. Several serological tests are of value in diagnosis.
Untreated, the infection is fatal within two years, in approximately 70 per cent of patients. Treatment traditionally involved sodium stibogluconate, but other chemotherapeutic agents (including allupurinol, ketoconazole, and immunotherapy) are now in use, the most recently used being liposomal amphotericin B. Although immunointact persons usually respond satisfactorily, they are likely to relapse if they have HIV infection (see AIDS/HIV).
Cutaneous leishmaniasis This form is caused by infection with L. tropica, L. major,
L. aethiopica, and other species. The disease is widely distributed in the Mediterranean region, Middle East, Asia, Africa, Central and South America, and the former Soviet Union. It is characterised by localised cutaneous ulcers
– usually situated on exposed areas of the body. Diagnosis is by demonstration of the causative organism in a skin biopsy-specimen; the leishmanin skin test is of value. Most patients respond to sodium stibogluconate (see above); local heat therapy is also used. Paromomycin cream has been successfully applied locally.
Mucocutaneous leishmaniasis This form is caused by L. braziliensis and rarely L. mexicana. It is present in Central and South America, particularly the Amazon basin, and characterised by highly destructive, ulcerative, granulomatous lesions of the skin and mucous membranes, especially involving the mucocutaneous junctions of the mouth, nasopharynx, genitalia, and rectum. Infection is usually via a super?cial skin lesion at the site of a sand?y bite. However, spread is by haematogenous routes (usually after several years) to a mucocutaneous location. Diagnosis and treatment are the same as for cutaneous leishmaniasis.... leishmaniasis
The local effects of the tumour commonly cause headache and, less frequently, impairment of vision, particularly of the temporal ?eld of vision, as a result of pressure on the nerves to the eye. The tumour may damage the other pituitary cells giving rise to gonadal, thyroid or adrenocortical insu?ciency. The disease often becomes obvious in persons over about 45 years of age; they may also complain of excessive sweating, joint pains and lethargy. The diagnosis is con?rmed by measuring the level of growth hormone in the serum and by an X-ray of the skull which usually shows enlargement of the pituitary fossa.
Treatment The most e?ective treatment is surgically to remove the pituitary adenoma. This can usually be done through the nose and the sphenoid sinus, but large adenomas may need a full CRANIOTOMY. Surgery cures about 80 per cent of patients with a microadenoma and 40 per cent of those with a large lesion; the rate of recurrence is 5–10 per cent. For recurrences, or for patients un?t for surgery or who refuse it, a combination of irradiation and drugs may be helpful. Deep X-ray therapy to the pituitary fossa is less e?ective than surgery but may also be helpful, and recently more sophisticated X-ray techniques, such as gamma knife irradiation, have shown promise. Drugs – such as BROMOCRIPTINE, capergoline and quiangoline, which are dopamine agonists – lower growth-hormone levels in acromegaly and are particularly useful as an adjunct to radiotherapy. Drugs which inhibit growth-hormone release by competing for its receptors, octeotride and lanreotride, also have a place in treatment.
See www.niddk.nih.gov/health/endo/pubs/ acro/acro.htm
www.umm.edu/endocrin/acromegaly.htm... acromegaly
Extrinsic allergic alveolitis is the condition induced by the lungs becoming allergic (see ALLERGY) to various factors or substances. It includes BAGASSOSIS, FARMER’S LUNG and BUDGERIGAR-FANCIER’S LUNG, and is characterised by the onset of shortness of breath, tightness of the chest, cough and fever. The onset may be sudden or gradual. Treatment consists of removal of the affected individual from the o?ending material to which he or she has become allergic. CORTICOSTEROIDS give temporary relief.
Fibrosing alveolitis In this disease there is di?use FIBROSIS of the walls of the alveoli of the lungs. This causes loss of lung volume with both forced expiratory volume and vital capacity affected, but the ratio between them remaining normal. The patient complains of cough and progressive DYSPNOEA. Typically the patient will be cyanosed (blue – see CYANOSIS), clubbed (see CLUBBING), and have crackles in the mid- and lower-lung ?elds. Blood gases will reveal HYPOXIA and, in early disease, hypocapnia (de?ciency of carbon dioxide in the blood due to hyperventilation). There is an association with RHEUMATOID ARTHRITIS (about one-eighth of cases), systemic lupus erythematosus (see under LUPUS), and systemic SCLEROSIS. Certain drugs – for example, bleomycin, busulphan and hexamethonium – may also cause this condition, as may high concentrations of oxygen, and inhalation of CADMIUM fumes.... alveolitis
The toxin has two components, one having haemagglutinin activity and the other neurotoxic activity which produces most of the symptoms. It has a lethal dose of as little as 1 mg/kg and is highly selective for cholinergic nerves. Thus the symptoms are those of autonomic parasympathetic blockade (dry mouth, constipation, urinary retention, mydriasis, blurred vision) and progress to blockade of somatic cholinergic transmission (muscle weakness). Death results from respiratory muscle paralysis. Treatment consists of supportive measures and 4 aminopyridine and 3, 4 di-aminopyridine, which may antagonise the e?ect of the toxin.... botulism
Shigellosis This form is usually caused by Shigella dysenteriae-1 (Shiga’s bacillus), Shigella ?exneri, Shigella boydii, and Shigella sonnei; the latter is the most benign and occurs in temperate climates also. It is transmitted by food and water contamination, by direct contact, and by ?ies; the organisms thrive in the presence of overcrowding and insanitary conditions. The incubation is between one and seven days, and the severity of the illness depends on the strain responsible. Duration of illness varies from a few days to two weeks and can be particularly severe in young, old, and malnourished individuals. Complications include perforation and haemorrhage from the colo-rectum, the haemolytic uraemic syndrome (which includes renal failure), and REITER’S SYNDROME. Diagnosis is dependent on demonstration of Shigella in (a) faecal sample(s) – before or usually after culture.
If dehydration is present, this should be treated accordingly, usually with an oral rehydration technique. Shigella is eradicated by antibiotics such as trimethoprimsulphamethoxazole, trimethoprim, ampicillin, and amoxycillin. Recently, a widespread resistance to many antibiotics has developed, especially in Asia and southern America, where the agent of choice is now a quinolone compound, for example, cipro?oxacin; nalidixic acid is also e?ective. Prevention depends on improved hygiene and sanitation, careful protection of food from ?ies, ?y destruction, and garbage disposal. A Shigella carrier must not be allowed to handle food.
Entamoeba histolytica infection Most cases occur in the tropics and subtropics. Dysentery may be accompanied by weight loss, anaemia, and occasionally DYSPNOEA. E. histolytica contaminates food (e.g. uncooked vegetables) or drinking water. After ingestion of the cyst-stage, and following the action of digestive enzymes, the motile trophozoite emerges in the colon causing local invasive disease (amoebic colitis). On entering the portal system, these organisms may gain access to the liver, causing invasive hepatic disease (amoebic liver ‘abscess’). Other sites of ‘abscess’ formation include the lungs (usually right) and brain. In the colo-rectum an amoeboma may be di?cult to di?erentiate from a carcinoma. Clinical symptoms usually occur within a week, but can be delayed for months, or even years; onset may be acute – as for Shigella spp. infection. Perforation, colo-rectal haemorrhage, and appendicitis are unusual complications. Diagnosis is by demonstration of E. histolytica trophozoites in a fresh faecal sample; other amoebae affecting humans do not invade tissues. Research techniques can be used to di?erentiate between pathogenic (E. dysenteriae) and non-pathogenic strains (E. dispar). Alternatively, several serological tests are of value in diagnosis, but only in the presence of invasive disease.
Treatment consists of one of the 5nitroimidazole compounds – metronidazole, tinidazole, and ornidazole; alcohol avoidance is important during their administration. A ?ve- to ten-day course should be followed by diloxanide furoate for ten days. Other compounds – emetine, chloroquine, iodoquinol, and paromomycin – are now rarely used. Invasive disease involving the liver or other organ(s) usually responds favourably to a similar regimen; aspiration of a liver ‘abscess’ is now rarely indicated, as controlled trials have indicated a similar resolution rate whether this technique is used or not, provided a 5-nitroimidazole compound is administered.... dysentery
– there may be epidemics spread by the bite of mosquitoes or ticks.
The clinical features begin with in?uenza-like symptoms – aches, temperature and wretchedness; then the patient develops a headache with drowsiness, confusion and neck sti?ness. Severely ill patients develop changes in behaviour, abnormalities of speech, and deterioration, sometimes with epileptic seizures. Some develop paralysis and memory loss. CT (see COMPUTED TOMOGRAPHY) and MRI brain scans show brain swelling, and damage to the temporal lobes if the herpes virus is involved. ELECTROENCEPHALOGRAPHY (EEG), which records the brainwaves, is abnormal. Diagnosis is possible by an examination of the blood or other body ?uids for antibody reaction to the virus, and modern laboratory techniques are very speci?c.
In general, drugs are not e?ective against viruses – antibiotics are of no use. Herpes encephalitis does respond to treatment with the antiviral agent, aciclovir. Treatment is supportive: patients should be given painkillers, and ?uid replacement drugs to reduce brain swelling and counter epilepsy if it occurs. Fortunately, most sufferers from encephalitis make a complete recovery, but some are left severely disabled with physical defects, personality and memory disturbance, and epileptic ?ts. Rabies is always fatal and the changes found in patients with AIDS are almost always progressive. Except in very speci?c circumstances, it is not possible to be immunised against encephalitis.
Encephalitis lethargica is one, now rare, variety that reached epidemic levels after World War I. It was characterised by drowsiness and headache leading on to COMA. The disease occasionally occurs as a complication after mumps and sometimes affected individuals subsequently develop postencephalitic PARKINSONISM.... encephalitis
Staphylococcal food poisoning occurs after food such as meat products, cold meats, milk, custard and egg products becomes contaminated before or after cooking, usually through incorrect handling by humans who carry S. aureus. The bacteria produce an ENTEROTOXIN which causes the symptoms of food poisoning 1–8 hours after ingestion. The toxin can withstand heat; thus, subsequent cooking of contaminated food will not prevent illness.
Heat-resistant strains of Cl. perfringens cause food poisoning associated with meat dishes, soups or gravy when dishes cooked in bulk are left unrefrigerated for long periods before consumption. The bacteria are anaerobes (see ANAEROBE) and form spores; the anaerobic conditions in these cooked foods allow the germinated spores to multiply rapidly during cooling, resulting in heavy contamination. Once ingested the bacteria produce enterotoxin in the intestine, causing symptoms within 8–24 hours.
Many di?erent types of Salmonella (about 2,000) cause food poisoning or ENTERITIS, from eight hours to three days after ingestion of food in which they have multiplied. S. brendeny, S. enteritidis, S. heidelberg, S. newport and S. thompson are among those commonly causing enteritis. Salmonella infections are common in domesticated animals such as cows, pigs and poultry whose meat and milk may be infected, although the animals may show no symptoms. Duck eggs may harbour Salmonella (usually S. typhimurium), arising from surface contamination with the bird’s faeces, and foods containing uncooked or lightly cooked hen’s eggs, such as mayonnaise, have been associated with enteritis. The incidence of human S. enteritidis infection has been increasing, by more than 15-fold in England and Wales annually, from around 1,100 a year in the early 1980s to more than 32,000 at the end of the 1990s, but has since fallen to about 10,000. A serious source of infection seems to be poultry meat and hen’s eggs.
Although Salmonella are mostly killed by heating at 60 °C for 15 minutes, contaminated food requires considerably longer cooking and, if frozen, must be completely thawed beforehand, to allow even cooking at a su?cient temperature.
Enteritis caused by Campylobacter jejuni is usually self-limiting, lasting 1–3 days. Since reporting of the disease began in 1977, in England and Wales its incidence has increased from around 1,400 cases initially to nearly 13,000 in 1982 and to over 42,000 in 2004. Outbreaks have been associated with unpasteurised milk: the main source seems to be infected poultry.
ESCHERICHIA COLI O157 was ?rst identi?ed as a cause of food poisoning in the early 1980s, but its incidence has increased sharply since, with more than 1,000 cases annually in the United Kingdom in the late 1990s. The illness can be severe, with bloody diarrhoea and life-threatening renal complications. The reservoir for this pathogen is thought to be cattle, and transmission results from consumption of raw or undercooked meat products and raw dairy products. Cross-infection of cooked meat by raw meat is a common cause of outbreaks of Escherichia coli O157 food poisoning. Water and other foods can be contaminated by manure from cattle, and person-to-person spread can occur, especially in children.
Food poisoning associated with fried or boiled rice is caused by Bacillus cereus, whose heat-resistant spores survive cooking. An enterotoxin is responsible for the symptoms, which occur 2–8 hours after ingestion and resolve after 8–24 hours.
Viruses are emerging as an increasing cause of some outbreaks of food poisoning from shell?sh (cockles, mussels and oysters).
The incidence of food poisoning in the UK rose from under 60,000 cases in 1991 to nearly 79,000 in 2004. Public health measures to control this rise include agricultural aspects of food production, implementing standards of hygiene in abattoirs, and regulating the environment and process of industrial food production, handling, transportation and storage.... food poisoning
Causes These include injury – especially that sustained in war – disease, FROSTBITE, severe burns, ATHEROMA in large blood vessels, and diseases such as DIABETES MELLITUS and RAYNAUD’S DISEASE. Gas gangrene is a form that occurs when injuries are infected with soil contaminated with gas-producing bacilli such as Clostridium welchii, which are found in well-cultivated ground.
Treatment Dry gangrene must be kept dry, and AMPUTATION of the dead tissue performed when a clear demarcation line with healthy tissue has formed. Wet gangrene requires urgent surgery and prompt use of appropriate antibiotics.... gangrene
Treatment Crusts should be gently removed with SALINE. Mild cases respond to frequent application of mupiricin or NEOMYCIN/BACITRACIN ointment; more severe cases should be treated orally or, sometimes, intravenously with FLUCLOXACILLIN or one of the CEPHALOSPORINS. If the patient is allergic to penicillin, ERYTHROMYCIN can be used.
For severe, intractable cases, an oral retinoid drug called isotretinoin (commercially produced as Roaccutane®) can be used. It is given systemically but treatment must be supervised by a consultant dermatologist as serious side-effects, including possible psychiatric disturbance, can occur. The drug is also teratogenic (see TERATOGENESIS), so women who are, or who may become, pregnant must not take isotretinoin. It acts mainly by suppressing SEBUM production in the sebaceous glands and can be very e?ective. Recurrent bouts of impetigo should raise suspicion of underlying SCABIES or head lice. Bactericidal soaps and instilling an antibiotic into the nostrils may also help.... impetigo
W. bancrofti in that it is shorter and thicker, and is found in the bloodstream during the day, not at night. It is transmitted by the mango ?y, Chrysops dimidiata, but other ?ies of this genus can also transmit it. It is con?ned to West and Central Africa. The characteristic feature of the disease is the appearance of fugitive swellings which may arise anywhere in the body in the course of the worm’s migration through it: these are known as Calabar swellings. The worm is often found in the eye, hence the old name of the worm in Africa – the eye worm. Diethylcarbamazine is the treatment for this form of FILARIASIS.... loiasis
Bacterial meningitis is life-threatening: in the United Kingdom, 5–10 per cent of children who contract the disease may die. Most cases of acute bacterial meningitis in the UK are caused by two bacteria: Neisseria meningitidis (meningococcus), and Streptococcus pneumoniae (pneumococcus); other bacteria include Haemophilus in?uenzae (a common cause until virtually wiped out by immunisation), Escherichia coli, Mycobacterium tuberculosis (see TUBERCULOSIS), Treponema pallidum (see SYPHILIS) and Staphylococci spp. Of the bacterial infections, meningococcal group B is the type that causes a large number of cases in the UK, while group A is less common.
Bacterial meningitis may occur by spread from nearby infected foci such as the nasopharynx, middle ear, mastoid and sinuses (see EAR, DISEASES OF). Direct infection may be the result of penetrating injuries of the skull from accidents or gunshot wounds. Meningitis may also be a complication of neurosurgery despite careful aseptic precautions. Immuno-compromised patients – those with AIDS or on CYTOTOXIC drugs – are vulnerable to infections.
Spread to contacts may occur in schools and similar communities. Many people harbour the meningococcus without developing meningitis. In recent years small clusters of cases, mainly in schoolchildren and young people at college, have occurred in Britain.
Symptoms include malaise accompanied by fever, severe headache, PHOTOPHOBIA, vomiting, irritability, rigors, drowsiness and neurological disturbances. Neck sti?ness and a positive KERNIG’S SIGN appearing within a few hours of infection are key diagnostic signs. Meningococcal and pneumococcal meningitis may co-exist with SEPTICAEMIA, a much more serious condition in terms of death rate or organ damage and which constitutes a grave emergency demanding rapid treatment.
Diagnosis and treatment are urgent and, if bacterial meningitis is suspected, antibiotic treatment should be started even before laboratory con?rmation of the infection. Analysis of the CEREBROSPINAL FLUID (CSF) by means of a LUMBAR PUNCTURE is an essential step in diagnosis, except in patients for whom the test would be dangerous as they have signs of raised intracranial pressure. The CSF is clear or turbid in viral meningitis, turbid or viscous in tuberculous infection and turbulent or purulent when meningococci or staphylococci are the infective agents. Cell counts and biochemical make-up of the CSF are other diagnostic pointers. Serological tests are done to identify possible syphilitic infection, which is now rare in Britain.
Patients with suspected meningitis should be admitted to hospital quickly. General pracitioners are encouraged to give a dose of intramuscular penicillin before sending the child to hospital. Treatment in hospital is usually with a cephalosporin, such as ceftazidime or ceftriaxone. Once the sensitivity of the organism is known as a result of laboratory studies on CSF and blood, this may be changed to penicillin or, in the case of H. in?uenzae, to amoxicillin. Local infections such as SINUSITIS or middle-ear infection require treatment, and appropriate surgery for skull fractures or meningeal tears should be carried out as necessary. Tuberculous meningitis is treated for at least nine months with anti-tuberculous drugs (see TUBERCULOSIS). If bacterial meningitis causes CONVULSIONS, these can be controlled with diazepam (see TRANQUILLISERS; BENZODIAZEPINES) and ANALGESICS will be required for the severe headache.
Coexisting septicaemia may require full intensive care with close attention to intravenous ?uid and electrolyte balance, control of blood clotting and blood pressure.
Treatment of close contacts such as family, school friends, medical and nursing sta? is recommended if the patient has H. in?uenzae or N. meningitidis: RIFAMPICIN provides e?ective prophylaxis. Contacts of patients with pneumococcal infection do not need preventive treatment. Vaccines for meningococcal meningitis may be given to family members in small epidemics and to any contacts who are especially at risk such as infants, the elderly and immuno-compromised individuals.
The outlook for a patient with bacterial meningitis depends upon age – the young and old are vulnerable; speed of onset – sudden onset worsens the prognosis; and how quickly treatment is started – hence the urgency of diagnosis and admission to hospital. Recent research has shown that children who suffer meningitis in their ?rst year of life are ten times more likely to develop moderate or severe disability by the age of ?ve than contemporaries who have not been infected. (See British Medical Journal, 8 September 2001, page 523.)
Prevention One type of bacterial meningitis, that caused by Haemophilus, has been largely controlled by IMMUNISATION; meningococcal C vaccine has largely prevented this type of the disease in the UK. So far, no vaccine against group B has been developed, but research continues. Information on meningitis can be obtained from the Meningitis Trust and the Meningitis Research Foundation.... meningitis
Chronic paronychia occurs with reinfection of the nail bed. This is usually because the person’s hands are regularly immersed in water, making the skin vulnerable to infection. The ?nger should be kept dry and a dry dressing applied accompanied by a course of antibiotics
– FLUCLOXACILLIN or a cephalosporin.... paronychia
– is caused by the bacterium Yersinis pestis. Plague remains a major infection in many tropical countries.
The reservoir for the bacillus in urban infection lies in the black rat (Rattus rattus), and less importantly the brown (sewer) rat (Rattus norvegicus). It is conveyed to humans by the rat ?ea, usually Xenopsylla cheopis: Y. pestis multiplies in the gastrointestinal tract of the ?ea, which may remain infectious for up to six weeks. In the pneumonic form (see below), human-to-human transmission can occur by droplet infection. Many lower mammals (apart from the rat) can also act as a reservoir in sylvatic transmission which remains a major problem in the US (mostly in the south-western States); ground-squirrels, rock-squirrels, prairie dogs, bobcats, chipmunks, etc. can be affected.
Clinically, symptoms usually begin 2–8 days after infection; disease begins with fever, headache, lassitude, and aching limbs. In over two-thirds of patients, enlarged glands (buboes) appear – usually in the groin, but also in the axillae and cervical neck; this constitutes bubonic plague. Haemorrhages may be present beneath the skin causing gangrenous patches and occasionally ulcers; these lesions led to the epithet ‘Black Death’. In a favourable case, fever abates after about a week, and the buboes discharge foul-smelling pus. In a rapidly fatal form (septicaemic plague), haematogenous transmission produces mortality in a high percentage of cases. Pneumonic plague is associated with pneumonic consolidation (person-to-person transmission) and death often ensues on the fourth or ?fth day. (The nursery rhyme ‘Ringo-ring o’ roses, a pocketful o’ posies, atishoo! atishoo!, we all fall down’ is considered to have originated in the 17th century and refers to this form of the disease.) In addition, meningitic and pharyngeal forms of the disease can occur; these are unusual. Diagnosis consists of demonstration of the causative organism.
Treatment is with tetracycline or doxycycline; a range of other antibiotics is also e?ective. Plague remains (together with CHOLERA and YELLOW FEVER) a quarantinable disease. Contacts should be disinfected with insecticide powder; clothes, skins, soft merchandise, etc. which have been in contact with the infection can remain infectious for several months; suspect items should be destroyed or disinfected with an insecticide. Ships must be carefully checked for presence of rats; the rationale of anchoring a distance from the quay prevents access of vermin. (See also EPIDEMIC; PANDEMIC; NOTIFIABLE DISEASES.)... plague
Pneumonia with no predisposing cause – community-acquired pneumonia – is caused most often by Streptococcus pneumoniae (PNEUMOCOCCUS). The other most common causes are viruses, Mycoplasma pneumoniae and Legionella species (Legionnaire’s disease). Another cause, Chlamydia psittaci, may be associated with exposure to perching birds.
In patients with underlying lung disease, such as CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) or BRONCHIECTASIS as in CYSTIC FIBROSIS, other organisms such as Haemophilus in?uenzae, Klebsiella, Escherichia coli and Pseudomonas aeruginosa are more prominent. In patients in hospital with severe underlying disease, pneumonia, often caused by gram-negative bacteria (see GRAM’S STAIN), is commonly the terminal event.
In patients with an immune system suppressed by pregnancy and labour, infection with HIV, CHEMOTHERAPY or immunosuppressive drugs after organ transplantation, a wider range of opportunistic organisms needs to be considered. Some of these organisms such as CYTOMEGALOVIRUS (CMV) or the fungus Pneumocystis carinii rarely cause disease in immunocompetent individuals – those whose body’s immune (defence) system is e?ective.
TUBERCULOSIS is another cause of pneumonia, although the pattern of lung involvement and the more chronic course usually di?erentiate it from other causes of pneumonia.
Symptoms The common symptoms of pneumonia are cough, fever (sometimes with RIGOR), pleuritic chest pain (see PLEURISY) and shortness of breath. SPUTUM may not be present at ?rst but later may be purulent or reddish (rusty).
Examination of the chest may show the typical signs of consolidation of an area of lung. The solid lung in which the alveoli are ?lled with in?ammatory exudate is dull to percussion but transmits sounds better than air-containing lung, giving rise to the signs of bronchial breathing and increased conduction of voice sounds to the stethoscope or palpating hand.
The chest X-ray in pneumonia shows opacities corresponding to the consolidated lung. This may have a lobar distribution ?tting with limitation to one area of the lung, or have a less con?uent scattered distribution in bronchopneumonia. Blood tests usually show a raised white cell (LEUCOCYTES) count. The organism responsible for the pneumonia can often be identi?ed from culture of the sputum or the blood, or from blood tests for the speci?c ANTIBODIES produced in response to the infection.
Treatment The treatment of pneumonia involves appropriate antibiotics together with oxygen, pain relief and management of any complications that may arise. When treatment is started, the causative organism has often not been identi?ed so that the antibiotic choice is made on the basis of the clinical features, prevalent organisms and their sensitivities. In severe cases of community-acquired pneumonia (see above), this will often be a PENICILLIN or one of the CEPHALOSPORINS to cover Strep. pneumoniae together with a macrolide such as ERYTHROMYCIN. Pleuritic pain will need analgesia to allow deep breathing and coughing; oxygen may be needed as judged by the oxygen saturation or blood gas measurement.
Possible complications of pneumonia are local changes such as lung abscess, pleural e?usion or EMPYEMA and general problems such as cardiovascular collapse and abnormalities of kidney or liver function. Appropriate treatment should result in complete resolution of the lung changes but some FIBROSIS in the lung may remain. Pneumonia can be a severe illness in previously ?t people and it may take some months to return to full ?tness.... pneumonia
Louse-borne relapsing fever is an EPIDEMIC disease, usually associated with wars and famines, which has occurred in practically every country in the world. For long confused with TYPHUS FEVER and typhoid fever (see ENTERIC FEVER), it was not until the 1870s that the causal organism was described by Obermeier. It is now known as the Borrelia recurrentis, a motile spiral organism 10–20 micrometres in length. The organism is transmitted from person to person by the louse, Pediculus humanus.
Symptoms The incubation period is up to 12 days (but usually seven). The onset is sudden, with high temperature, generalised aches and pains, and nose-bleeding. In about half of cases, a rash appears at an early stage, beginning in the neck and spreading down over the trunk and arms. JAUNDICE may occur; and both the LIVER and the SPLEEN are enlarged. The temperature subsides after ?ve or six days, to rise again in about a week. There may be up to four such relapses (see the introductory paragraph above).
Treatment Preventive measures are the same as those for typhus. Rest in bed is essential, as are good nursing and a light, nourishing diet. There is usually a quick response to PENICILLIN; the TETRACYCLINES and CHLORAMPHENICOL are also e?ective. Following such treatment the incidence of relapse is about 15 per cent. The mortality rate is low, except in a starved population.
Tick-borne relapsing fever is an ENDEMIC disease which occurs in most tropical and sub-tropical countries. The causative organism is Borrelia duttoni, which is transmitted by a tick, Ornithodorus moubata. David Livingstone suggested that it was a tick-borne disease, but it was not until 1905 that Dutton and Todd produced the de?nitive evidence.
Symptoms The main di?erences from the louse-borne disease are: (a) the incubation period is usually shorter, 3–6 days (but may be as short as two days or as long as 12); (b) the febrile period is usually shorter, and the afebrile periods are more variable in duration, sometimes only lasting for a day or two; (c) relapses are much more numerous.
Treatment Preventive measures are more di?cult to carry out than in the case of the louse-borne infection. Protective clothing should always be worn in ‘tick country’, and old, heavily infected houses should be destroyed. Curative treatment is the same as for the louse-borne infection.... relapsing fever
Symptoms The period of incubation (i.e. the time elapsing between the reception of infection and the development of symptoms) varies somewhat. In most cases it lasts only two to three days, but in occasional cases the patient may take a week to develop his or her ?rst symptoms. The occurrence of fever is usually short and sharp, with rapid rise of temperature to 40 °C (104 °F), shivering, vomiting, headache, sore throat and marked increase in the rate of the pulse. In young children, CONVULSIONS or DELIRIUM may precede the fever. The rash usually appears within 24 hours of the onset of fever and lasts about a week.
Complications The most common and serious of these is glomerulonephritis (see under KIDNEYS, DISEASES OF), which may arise during any period in the course of the fever, but particularly when DESQUAMATION occurs. Occasionally the patient develops chronic glomerulonephritis. Another complication is infection of the middle ear (otitis media – see under EAR, DISEASES OF). Other disorders affecting the heart and lungs occasionally arise in connection with scarlet fever, the chief of these being ENDOCARDITIS, which may lay the foundation of valvular disease of the heart later in life. ARTHRITIS may produce swelling and pain in the smaller rather than in the larger joints; this complication usually occurs in the second week of illness. Scarlet fever, which is now a mild disease in most patients, should be treated with PENICILLIN.... scarlet fever
Causes The disease is caused by the bacillus Clostridium tetani, found generally in earth and dust and especially in places where animal manure is collected. Infection usually follows a wound, especially a deeply punctured or gunshot wound, with the presence of some foreign body. It is a hazard in war and also among farmers, gardeners and those in the construction industry. The bacillus develops a toxin in the wound, which is absorbed through the motor nerves into the spinal cord where it renders the nerves excitable and acutely sensitive to mild stimuli.
Symptoms Most commonly appearing within four to ?ve days of the wound, the patient’s symptoms may be delayed for several weeks – by which time the wound may have healed. Initially there is muscle sti?ness around the wound followed by sti?ness around the jaw, leading to lockjaw, or trismus. This extends to the muscles of the neck, back, chest, abdomen, and limbs, leading to strange, often changing, contorted postures, accompanied by frequent seizures – often provoked by quite minor stimuli such as a sudden noise. The patient’s breathing may be seriously affected, in severe cases leading to ASPHYXIA; the temperature may rise sharply, often with sweating; and severe pain is common. Mental clarity is characteristic adding to the patient’s anxiety. In severe infections death may be from asphyxia, PNEUMONIA, or general exhaustion. More commonly, the disease takes a chronic course, leading to gradual recovery. Outcome depends on several factors, chie?y the patient’s immune status and age, and early administration of appropriate treatment.
Tetanus may occur in newborn babies, particularly when birth takes place in an unhygienic environment. It is particularly common in the tropics and developing countries, with a high mortality rate. Local tetanus is a rare manifestation, in which only muscles around the wound are affected, though sti?ness may last for several months. STRYCHNINE poisoning and RABIES, although similar in some respects to tetanus, may be easily distinguished by taking a good history.
Prevention and treatment The incidence of tetanus in the United Kingdom has been almost abolished by the introduction of tetanus vaccine (see IMMUNISATION). Children are routinely immunised at two, three and four months of age, and boosters are given later in life to at-risk workers, or those travelling to tropical parts.
Treatment should be started as soon as possible after sustaining a potentially dangerous wound. An intravenous injection of antitoxin should be given immediately, the wound thoroughly cleaned and PENICILLIN administered. Expert nursing is most important. Spasms may be minimised by reducing unexpected stimuli, and diazepam (see BENZODIAZEPINES; TRANQUILLISERS) is helpful. Intravenous feeding should be started immediately if the patient cannot swallow. Aspiration of bronchial secretions and antibiotic treatment of pneumonia may be necessary.... tetanus
Clinically, yellow fever is characterised by jaundice, fever, chills, headache, gastrointestinal haemorrhage(s), and ALBUMINURIA. The incubation period is 3–6 (up to 10) days. Differentiation from viral hepatitides, other viral haemorrhagic fevers, severe Plasmodium falciparum malaria, and several other infections is often impossible without sophisticated investigative techniques. Infection carries a high mortality rate. Liver histology (biopsy is contraindicated due to the haemorrhagic diathesis) shows characteristic changes; a fulminating hepatic infection is often present. Acute in?ammation of the kidneys and an in?amed, congested gastric mucosa, often accompanied by haemorrhage, are also demonstrable; myocardial involvement often occurs. Diagnosis is primarily based on virological techniques; serological tests are also of value. Yellow fever should be suspected in any travellers from an endemic area.
Management consists of instituting techniques for acute hepatocellular (liver-cell) failure. The affected individual should be kept in an isolation unit, away from mosquitoes which could transmit the disease to a healthy individual. Formerly, laboratory infections were occasionally acquired from infected blood samples. Prophylactically, a satisfactory attenuated VACCINE (17D) has been available for around 60 years; this is given subcutaneously and provides an individual with excellent protection for ten years; international certi?cates are valid for this length of time. Every traveller to an endemic area should be immunised; this is mandatory for entry to countries where the infection is endemic.... yellow fever
Three forms: major (grand mal); temporal lobe; and minor (petit mal). In petit mal the period of unconsciousness consists of brief absences lasting less than 15 seconds.
Treatment. Orthodox medical: Carbamazepine, phenytoin and many other drugs.
Alternatives. BHP (1983) recommends: Grand mal: Passion flower, Skullcap, Verbena. Petit mal: Hyssop. Standard central nervous system relaxants are Hops, Lobelia, Passion flower, Vervain, Valerian, Skullcap. Wm Boericke used Mugwort. Peony leaf tea had a long traditional use. In nearly all epileptics there is functional heart disturbance (Hawthorn, Lily of the Valley, Motherwort). Mistletoe can help in the struggle to control seizures and improve the quality of life.
Two important remedies are Skullcap and Passion flower. Both work quickly without risk of respiratory arrest. If dose by mouth is not possible insert gelatin capsules containing powders, per rectum, child or adult lying prone. This method is particularly suitable for feverish convulsions or Grand mal.
Repeat after 5 minutes if patient continues in convulsion. Where neither of these powders are available, Chamomile, Valerian or Mistletoe may be used.
“The remedy I have relied on most,” writes C.I. Reid, MD (Ellingwood’s Journal) “is Passion flower. Use this alone or in combination with Gelsemium – more often alone. I cannot say I obtain an absolutely curative effect, but the spasms disappear and do not return while the remedy is continued. It has none of the unpleasant effects of other medicines. I give the liquid extract in doses from 25-30 drops, 3-4 times daily, for continued use. It may be given more frequently for convulsions.”
Alfred Dawes, MNIMH. Green tincture of Mistletoe, 3-5 drops. Or, combine equal parts: Liquid Extract Skullcap, Valerian and Black Horehound.
Finlay Ellingwood MD combines White Bryony, Prickly Ash, Skullcap and St John’s Wort.
Samuel Thomson MD. Lobelia 2; Cayenne 1; (antispasmodic drops) given at the premonitary stage. 1-2 teaspoons.
Edgar Cayce. Passion flower tea. Hot Castor oil packs.
Excess acidity and intestinal toxaemia. There is considerable opinion that these trigger an attack. Combination: Liquid Extracts – Skullcap 15ml; Mistletoe 10ml; Meadowsweet 10ml; Elderflowers 10ml. Two 5ml teaspoons in water thrice daily.
West African Black Pepper. (Piper guineense) is used by traditional Nigerian healers to good effect. Associated with imperfect menstruation. Liquid Extracts, single or in combination: Black Cohosh, Life root, Lobelia. Dose: 5-15 drops thrice daily.
Associated with mental weakness. Liquid Extract Oats (avena sativa). 2-3 teaspoons in water thrice daily.
Aromatherapy. (Complex partial seizures) Massage with essential oils found to be beneficial. (The Lancet, 1990, 336 (8723) 1120)
Diet. Salt-free lacto-vegetarian. Oatmeal porridge. A cleansing 8-day grape juice fast has its advocates. Vitamin E. In 24 epileptic children refractory to anti-epileptic drugs (AEDs) with generalised tonic- clonic and other types of seizures, addition of Vitamin E 400iu daily to existing AEDs was accompanied by a significant reduction in 10 of 12 cases. (Epilepsy 1989; 30(1): 84-89)
Supportives: osteopathic or chiropractic adjustments.
Note: A number of Italian physicians linked a salt-rich diet with epileptic fits. Number and violence diminished when discontinued and did not recur for weeks. Dr W.P. Best found that, in children, circumcism made a valuable contribution.
Drug-dependency. Herbal medication may offer a supportive role to primary medical treatment. Under no circumstances should sufferers discontinue basic orthodox treatments except upon the advice of a physician.
Information. British Epilepsy Association, 40 Hanover Square, Leeds LS3 1BE, UK. Send SAE.
To be treated by or in liaison with a qualified medical practitioner. ... epilepsy
Cup of Chamomile, Balm, or Meadowsweet tea. Liquorice helpful, but most popular is Ginger taken in the form of Ginger wine, or powdered root (quarter to half a teaspoon). Chrystalised Ginger from sweetshop is one of the safest and cheapest: 2-3 pieces sucked or chewed half hour before journey and at intervals thereafter.
Avoid tobacco which reduces oxygen count. Potter’s Ginger root capsules.
Peppermint. Before travelling, glass water with 2 drops.
Aromatherapy. Inhalant. 2-3 drops Peppermint oil on tissue.
Diet. No alcohol or fatty foods. Accept Papaya fruit, Lemons or Lemon juice, Honey, Acidophilus. Supplements. Alternatives to the above. Seven days before journey: B-complex, magnesium 200mg, calcium 400mg. ... motion sickness
Pleurisy causes short, rapid breathing to avoid the pain of deep inspiration.
Narrowing of the air passages may produce sudden and alarming attacks of di?cult breathing, especially among children – for example, in CROUP, asthma and DIPHTHERIA.
Most cardiac disorders (see HEART, DISEASES OF) cause breathlessness, especially when the person undergoes any special exertion.
Anaemia is a frequent cause.
Obesity is often associated with shortness of breath. Mountain climbing may cause breathlessness
because, as altitude increases, the amount of oxygen in the air falls (see ALTITUDE SICKNESS). (See also LUNGS and RESPIRATION.)... breathlessness
In recent years persistent child abuse in some children’s homes has come to light, with widespread publicity following o?enders’ appearances in court. Local communities have also protested about convicted paedophiles, released from prison, coming to live in their communities.
In England and Wales, local-government social-services departments are central in the prevention, investigation and management of cases of child abuse. They have four important protection duties laid down in the Children Act 1989. They are charged (1) to prevent children from suffering ill treatment and neglect; (2) to safeguard and promote the welfare of children in need; (3) when requested by a court, to investigate a child’s circumstances; (4) to investigate information – in concert with the NSPCC (National Society for the Prevention of Cruelty to Children) – that a child is suffering or is likely to suffer signi?cant harm, and to decide whether action is necessary to safeguard and promote the child’s welfare. Similar provisions exist in the other parts of the United Kingdom.
When anyone suspects that child abuse is occurring, contact should be made with the relevant social-services department or, in Scotland, with the children’s reporter. (See NONACCIDENTAL INJURY (NAI); PAEDOPHILIA.)... child abuse
Incubation period varies from a few hours to ?ve days. Watery diarrhoea may be torrential and the resultant dehydration and electrolyte imbalance, complicated by cardiac failure, commonly causes death. The victim’s skin elasticity is lost, the eyes are sunken, and the radial pulse may be barely perceptible. Urine production may be completely suppressed. Diagnosis is by detection of V. cholerae in a faecal sample. Treatment consists of rapid rehydration. Whereas the intravenous route may be required in a severe case, in the vast majority of patients oral rehydration (using an appropriate solution containing sodium chloride, glucose, sodium bicarbonate, and potassium) gives satisfactory results. Proprietary rehydration ?uids do not always contain adequate sodium for rehydration in a severe case. ANTIBIOTICS, for example, tetracycline and doxycycline, reduce the period during which V. cholerae is excreted (in children and pregnant women, furazolidone is safer); in an epidemic, rapid resistance to these, and other antibiotics, has been clearly demonstrated. Prevention consists of improving public health infrastructure – in particular, the quality of drinking water. When supplies of the latter are satisfactory, the infection fails to thrive. Though there have recently been large epidemics of cholera in much of South America and parts of central Africa and the Indian subcontinent, the risk of tourists and travellers contracting the disease is low if they take simple precautions. These include eating safe food (avoid raw or undercooked seafood, and wash vegetables in clean water) and drinking clean water. There is no cholera vaccine at present available in the UK as it provides little protection and cannot control spread of the disease. Those travelling to countries where it exists should pay scrupulous attention to food and water cleanliness and to personal hygiene.... cholera
Insulin-dependent and non-insulindependent diabetes have a varied pathological pattern and are caused by the interaction of several genetic and environmental factors.
Insulin-dependent diabetes mellitus (IDDM) (juvenile-onset diabetes, type 1 diabetes) describes subjects with a severe de?ciency or absence of insulin production. Insulin therapy is essential to prevent KETOSIS – a disturbance of the body’s acid/base balance and an accumulation of ketones in the tissues. The onset is most commonly during childhood, but can occur at any age. Symptoms are acute and weight loss is common.
Non-insulin-dependent diabetes mellitus (NIDDM) (maturity-onset diabetes, type 2 diabetes) may be further sub-divided into obese and non-obese groups. This type usually occurs after the age of 40 years with an insidious onset. Subjects are often overweight and weight loss is uncommon. Ketosis rarely develops. Insulin production is reduced but not absent.
A new hormone has been identi?ed linking obesity to type 2 diabetes. Called resistin – because of its resistance to insulin – it was ?rst found in mice but has since been identi?ed in humans. Researchers in the United States believe that the hormone may, in part, explain how obesity predisposes people to diabetes. Their hypothesis is that a protein in the body’s fat cells triggers insulin resistance around the body. Other research suggests that type 2 diabetes may now be occurring in obese children; this could indicate that children should be eating a more-balanced diet and taking more exercise.
Diabetes associated with other conditions (a) Due to pancreatic disease – for example, chronic pancreatitis (see PANCREAS, DISORDERS OF); (b) secondary to drugs – for example, GLUCOCORTICOIDS (see PANCREAS, DISORDERS OF); (c) excess hormone production
– for example, growth hormone (ACROMEGALY); (d) insulin receptor abnormalities; (e) genetic syndromes (see GENETIC DISORDERS).
Gestational diabetes Diabetes occurring in pregnancy and resolving afterwards.
Aetiology Insulin-dependent diabetes occurs as a result of autoimmune destruction of beta cells within the PANCREAS. Genetic in?uences are important and individuals with certain HLA tissue types (HLA DR3 and HLA DR4) are more at risk; however, the risks associated with the HLA genes are small. If one parent has IDDM, the risk of a child developing IDDM by the age of 25 years is 1·5–2·5 per cent, and the risk of a sibling of an IDDM subject developing diabetes is about 3 per cent.
Non-insulin-dependent diabetes has no HLA association, but the genetic in?uences are much stronger. The risks of developing diabetes vary with di?erent races. Obesity, decreased exercise and ageing increase the risks of disease development. The risk of a sibling of a NIDDM subject developing NIDDM up to the age of 80 years is 30–40 per cent.
Diet Many NIDDM diabetics may be treated with diet alone. For those subjects who are overweight, weight loss is important, although often unsuccessful. A diet high in complex carbohydrate, high in ?bre, low in fat and aiming towards ideal body weight is prescribed. Subjects taking insulin need to eat at regular intervals in relation to their insulin regime and missing meals may result in hypoglycaemia, a lowering of the amount of glucose in the blood, which if untreated can be fatal (see below).
Oral hypoglycaemics are used in the treatment of non-insulin-dependent diabetes in addition to diet, when diet alone fails to control blood-sugar levels. (a) SULPHONYLUREAS act mainly by increasing the production of insulin;
(b) BIGUANIDES, of which only metformin is available, may be used alone or in addition to sulphonylureas. Metformin’s main actions are to lower the production of glucose by the liver and improve its uptake in the peripheral tissues.
Complications The risks of complications increase with duration of disease.
Diabetic hypoglycaemia occurs when amounts of glucose in the blood become low. This may occur in subjects taking sulphonylureas or insulin. Symptoms usually develop when the glucose concentration falls below 2·5 mmol/l. They may, however, occur at higher concentrations in subjects with persistent hyperglycaemia – an excess of glucose – and at lower levels in subjects with persistent hypo-glycaemia. Symptoms include confusion, hunger and sweating, with coma developing if blood-sugar concentrations remain low. Re?ned sugar followed by complex carbohydrate will return the glucose concentration to normal. If the subject is unable to swallow, glucagon may be given intramuscularly or glucose intravenously, followed by oral carbohydrate, once the subject is able to swallow.
Although it has been shown that careful control of the patient’s metabolism prevents late complications in the small blood vessels, the risk of hypoglycaemia is increased and patients need to be well motivated to keep to their dietary and treatment regime. This regime is also very expensive. All risk factors for the patient’s cardiovascular system – not simply controlling hyperglycaemia – may need to be reduced if late complications to the cardiovascular system are to be avoided.
Diabetes is one of the world’s most serious health problems. Recent projections suggest that the disorder will affect nearly 240 million individuals worldwide by 2010 – double its prevalence in 1994. The incidence of insulin-dependent diabetes is rising in young children; they will be liable to develop late complications.
Although there are complications associated with diabetes, many subjects live normal lives and survive to an old age. People with diabetes or their relatives can obtain advice from Diabetes UK (www.diabetes.org.uk).
Increased risks are present of (a) heart disease, (b) peripheral vascular disease, and (c) cerebrovascular disease.
Diabetic eye disease (a) retinopathy, (b) cataract. Regular examination of the fundus enables any abnormalities developing to be detected and treatment given when appropriate to preserve eyesight.
Nephropathy Subjects with diabetes may develop kidney damage which can result in renal failure.
Neuropathy (a) Symmetrical sensory polyneuropathy; damage to the sensory nerves that commonly presents with tingling, numbness of pain in the feet or hands. (b) Asymmetrical motor diabetic neuropathy, presenting as progressive weakness and wasting of the proximal muscles of legs. (c) Mononeuropathy; individual motor or sensory nerves may be affected. (d) Autonomic neuropathy, which affects the autonomic nervous system, has many presentations including IMPOTENCE, diarrhoea or constipation and postural HYPOTENSION.
Skin lesions There are several skin disorders associated with diabetes, including: (a) necrobiosis lipoidica diabeticorum, characterised by one or more yellow atrophic lesions on the legs;
(b) ulcers, which most commonly occur on the feet due to peripheral vascular disease, neuropathy and infection. Foot care is very important.
Diabetic ketoacidosis occurs when there is insu?cient insulin present to prevent KETONE production. This may occur before the diagnosis of IDDM or when insu?cient insulin is being given. The presence of large amounts of ketones in the urine indicates excess ketone production and treatment should be sought immediately. Coma and death may result if the condition is left untreated.
Symptoms Thirst, POLYURIA, GLYCOSURIA, weight loss despite eating, and recurrent infections (e.g. BALANITIS and infections of the VULVA) are the main symptoms.
However, subjects with non-insulindependent diabetes may have the disease for several years without symptoms, and diagnosis is often made incidentally or when presenting with a complication of the disease.
Treatment of diabetes aims to prevent symptoms, restore carbohydrate metabolism to as near normal as possible, and to minimise complications. Concentration of glucose, fructosamine and glycated haemoglobin in the blood are used to give an indication of blood-glucose control.
Insulin-dependent diabetes requires insulin for treatment. Non-insulin-dependent diabetes may be treated with diet, oral HYPOGLYCAEMIC AGENTS or insulin.
Insulin All insulin is injected – mainly by syringe but sometimes by insulin pump – because it is inactivated by gastrointestinal enzymes. There are three main types of insulin preparation: (a) short action (approximately six hours), with rapid onset; (b) intermediate action (approximately 12 hours); (c) long action, with slow onset and lasting for up to 36 hours. Human, porcine and bovine preparations are available. Much of the insulin now used is prepared by genetic engineering techniques from micro-organisms. There are many regimens of insulin treatment involving di?erent combinations of insulin; regimens vary depending on the requirements of the patients, most of whom administer the insulin themselves. Carbohydrate intake, energy expenditure and the presence of infection are important determinants of insulin requirements on a day-to-day basis.
A new treatment for diabetes, pioneered in Canada and entering its preliminary clinical trials in the UK, is the transplantation of islet cells of Langerhans from a healthy person into a patient with the disorder. If the transplantation is successful, the transplanted cells start producing insulin, thus reducing or eliminating the requirement for regular insulin injections. If successful the trials would be a signi?cant advance in the treatment of diabetes.
Scientists in Israel have developed a drug, Dia Pep 277, which stops the body’s immune system from destroying pancratic ? cells as happens in insulin-dependent diabetes. The drug, given by injection, o?ers the possibility of preventing type 1 diabetes in healthy people at genetic risk of developing the disorder, and of checking its progression in affected individuals whose ? cells are already perishing. Trials of the drug are in progress.... diabetes mellitus
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