236 CHAPTER 5 Infectious diseases Tetanus ND An acute and often fatal disease, common in much of Asia, Africa, and South Amer ica, especially in neonates. Now rare in developed coun- tries: 30 \200\22340 cases/year in UK, many involving the elderly. Injecting drug users (eg those \200\230skin popping \200 \231) are also at particular risk. Spores of the Gram + ve organism Clostridium tetani (com mon in soil and animal feces) contaminate a wound, which may be trivial. The spores germina te in anaerobic conditions, producing tetanospasmin, an exotoxin which blocks inhibitory ne urones in the CNS and causes muscle spasm and rigidity. Incubation period is usually 4 \200\22314 days, but may be 1 day to 3 months. In 20 % of ca ses there is no known wound. Tetanus occasionally occurs after surgery or IM injections. Clinical features Stiffness of masseter muscles causes dif \201 culty in opening the mouth (trismus, lockjaw). Muscle stiffness may spread to all facial and skeletal muscles and mus cles of swallowing. Characteristically, the eyes are partly closed, the lips pursed and str etched (risus sardonicus). Spasm of chest muscles may restrict breathing. There may be abdo minal rigidity, stiff- ness of limbs and forced extension of the back (opisthotonus). In se vere cases, prolonged muscle spasms affect breathing and swallowing. Pyrexia is common. Aut onomic disturbances cause profuse sweating, tachycardia and hypertension, alternating with bradycardia and hypotension. Cardiac arrhythmias and arrest may occur. Differential diagnoses Dystonic reaction to metoclopramide or phenothiazines, strychnine po isoning, quinsy, dental abscess, meningitis, rabies. Procyclidine relieves muscle spasms fr om drug-induced dystonia, but will not affect tetanus; diazepam may relieve dystonia or tet anic spasms. Management Obtain senior medical and anesthetic help. Monitor breathing, ECG and BP. Refer to ICU. Control spasms with diazepam. Paralyze and ventilate if breathing becomes inadequat e. Clean and debride wounds. Give penicillin and metronidazole and human tetanus immune glo bulin. Prognosis Depends on severity of disease and quality of care. Short incubation (<4 days) an d rapid progression suggest severe disease with a high mortality. With expert intensive car e, the mortality in adults is <10 % , but neonatal tetanus is often fatal. Immunization Tetanus is eminently preventable by immunization and by proper care of wounds ( b p.406, b p.410). 237 BOTULISMND Gas gangrene This is a rapidly spreading infection of muscle caused by toxin-producing Clos tridial bacteria (anaerobic Gram + ve bacilli), usually C. perfringens . It is fatal if unt reated. It may involve wounds of the buttocks, amputa- tions for vascular disease or severe muscle injuries (eg gunshot wounds). Occasionally gas gangrene of the perineum occurs with out trauma. Incubation period is usually <4 days (sometimes a few hours). Sudden severe pai n occurs at the wound site. Generalized toxicity develops, with tachycardia, sweating and f ever. Swelling and skin discolouration occur around the wound, with a serous ooze, marked t enderness and sometimes haemorrhagic vesicles and crepitus. Shock and renal failure develop , with death often within 2 days of the \201 rst symptoms. Diagnosis depends on clinical features. Severe pain necessitates wound inspection (remove or window any plaster of paris (POP). Obtain immediate senior surgical advice if gas gangrene is suspected. The wound disc harge may contain Gram + ve bacilli. X-rays may show soft tissue gas, but its absence does not exclude gas gangrene. Treatment IV antibiotics (penicillin and clindamycin), immediate surgical removal of all infected tissue, and intensive care. Hyperbaric O 2 and gas gangren e antitoxin are rarely available and of no proven bene \201 t. Botulism ND The exotoxin of Clostridium botulinum paralyzes autonomic and motor nerves by b locking acetylcholine release at neuromuscular junctions and nerve synapses. Infection occu rs from eating tinned or preserved food contaminated with C. botulinum spores: cases have i nvolved sausage, tinned salmon, hazelnut yogurt and other foods. Rarely, C. botulinum infec ts wounds or colonizes the gut. Injecting drug users may develop botulism after IM or SC in jections of contaminated drugs. Incubation period is 12 \200\22372hr. Initial symptoms may be GI (nausea, vomiting, abdominal discomfort, dryness of the mouth) or neurological (dizzi ness, blurred vision, diplopia). Later problems include dysarthria, dysphagia, muscle weakn ess or paralysis, constipation and urinary retention, respiratory failure, and sudden death . Susceptibility varies: some people who eat contaminated food develop no symptoms or suffe r only mild fatigue. Clinical signs result from involvement of autonomic and motor nerves: dry mouth, cranial nerve palsies (ptosis, squint, \201 xed pupils, weakness of tongue), l imb weakness with \202 acid muscles. Consciousness and sensation are preserved. Hypotensi on and ileus may occur. Fever is unusual. Differential diagnoses are Guillain \200\223Barr syndrome, myasthenia, brainstem stroke, diphtheria, poisoning (anticholinergics or organo phosphates), paralytic rabies. Botulism may be misdiagnosed as staphylococcal food poisonin g, paralytic shell \201 sh poisoning, CO or mushroom poisoning. Management Get senior help . Assess breathing, ventilate if necessary and admit to ICU. Botulinum antitoxin reduces mo rtality and morbidity: see BNF and TOXBASE ( b p.181). Inform Public Health: others who hav e eaten contaminated food may need urgent treatment. Anticipate media enquiries and the arr ival of worried people with tins of suspicious food. 238 CHAPTER 5 Infectious diseases Sexually transmitted diseases The commonest sexually transmitted disease (STD) is non-speci \201 c genital infection. Other common diseases include chlamydia, gonorrhea, genital her pes, trichomoniasis, genital warts, pediculosis pubis, HIV, and syphilis. Many patients hav e more than one disease. Suspicion of STD necessi- tates prompt referral to a genitourinary (GU) medicine clinic for proper diagnosis, treatment and follow-up of the patient and cont acts. Some GU departments provide an on-call service. Only prescribe antibiotics for suspec ted STDs on the advice of a GU specialist. Genital ulcers and sores Most genital ulcers/erosions are either multiple and painful or si ngle and painless. In the UK, multiple genital ulcers are most often due to herpes simplex; other causes are Beh et \200\231s disease and (rarely) chancroid or scabies. Multiple pai nful sores may occur with gonorrhea, candida, or other conditions. Painless genital ulcerat ion should suggest syphilis (primary chancre is a single ulcer, secondary syphilis often mu ltiple: both are highly infectious and incidence has i recently). Other causes of painless ulcers include carcinoma and trauma (possibly self-in \202 icted). Urethritis In men, dysuria and urethral discharge are the commonest presenting symptoms of an STD. However, 5 \200\22310 % of men with gonococcal or non-gonococcal urethritis have no symptoms. Urethritis may result from physical trauma, foreign bodies or attempts at self-t reatment with intra- urethral chemicals. Gonorrhea usually has a shorter incubation period (3 \200\2235 days) than non- gonococcal u rethritis (eg chlamydia 7 \200\22314 days), but do not rely on a clinical diagnosis: refer to a GU clinic for diagnosis, management and follow-up. If no GU advice is available and tr eatment cannot wait for attendance at a GU clinic, give doxycycline 200mg PO stat and then 100mg PO daily (or tetracycline 500mg PO qds). If possible, make a glass slide of the disch arge, dried in air, for the patient to take to the clinic. He should be told not to pass ur ine for 4 hours before the appointment, in order to allow serial urine samples to be taken. Reiter \200\231s disease is a rare complication of non-gonococcal urethritis. There is arth ritis (mainly of knees, ankles and feet) and sometimes conjunctivitis, rashes and cardiac a nd neurological problems. Gonorrhea Gonorrhea may infect the urethra, cervix, rectum, pharynx or conjunc- tiva. Men u sually have dysuria and urethral discharge, with rectal discharge and tenesmus in homosexua ls. Women are often asymptomatic, but may have dysuria and vaginal discharge. Complications include prostatitis, epididymitis, salpingitis, Bartholin \200\231s abscess; rarely septicaemia with arthritis, fever, rash (maculopapular initially, then pustular) and endocarditis. 239 HEPATITIS AND LEPTOSPIROSIS Hepatitis ND Hepatitis A (infectious hepatitis) ND Hepatitis A occurs throughout the world, but is particularly common in the tropics and subtropics. It is transmitted by contaminati on of food or water with infected feces or urine. Many infections are asymptomatic. The inc ubation period is 2 \200\2236 weeks (usually 8 4 weeks). Fever, malaise, anorexia and nause a may last for 2 \200\2237 days before jaundice develops. Jaundice is more common in adults than in children and is associated with dark urine, pale stools and tender hepatomegaly. Treatment is symptomatic, but alcohol should be avoided. Infectivity is greatest before jau ndice develops, so isolation is of little value. Arrange follow-up by a specialist or GP. C omplete recovery is usual. Hepatitis A vaccine should be considered for close contacts (see BNF ). Hepatitis B ND Hepatitis B is transmitted by infected blood (eg shared needles in drug abus ers, tattooing, needlestick injury) and by sexual intercourse. The incuba- tion period is 6 weeks to 6 months. The symptoms are similar to hepatitis A, often with arthralgia and skin rashes. Most patients with hepatitis B recover completely. A few patients develop liver fa ilure or chronic hepatitis, with a risk of primary liver cancer. Refer to a specialist for follow-up. Asymptomatic carriers of hepatitis B virus are common ( 8 0.1 % of the populatio n in the UK, but 8 20 % in parts of Africa and Asia). Because of the high risk of infection , all health care workers should be immunized against hepatitis B and use \200\230standard precautions \200\231 ( b p.32) when handling all blood samples and \200\230sharps \200 \231. The management of needlestick injury is described on b p.418. Hepatitis C, D, and E N D Hepatitis C and D are spread in the same way as hepatitis B, and may cause hepatic failur e or chronic liver disease. No immunization is available. Hepatitis E is similar to hepatitis A, but has a high mortality in pregnancy. Refer to a sp ecialist for follow-up. Leptospirosis (Weil \200\231s disease) ND Leptospirosis, caused by the spirochaete Leptospi ra interrogans and other Leptospira species, is spread by contact with infected rat \200 \231s urine, often in rivers, canals or sewers. The leptospires enter the body through smal l breaks in the skin or via mucous membranes of the eyes or nose. About 10 days after expos ure (range 2 \200\22326 days) the illness starts with fever, severe muscle pains, headache, sore throat, nausea and vomiting. Conjunctival reddening is common. A haemorrhagic rash, j aundice, renal failure and pulmonary hemorrhage may occur (Weil \200\231s disease). Refer to an Infectious Diseases unit. Treatment is with penicillin or doxycycline with supp ortive care and haemodialysis if necessary. Prophylactic doxycycline is reasonable for peop le who fall into waterways likely to be contaminated with leptospires. 240 CHAPTER 5 Infectious diseases Herpes virus infections Varicella zoster Chickenpox results from primary infection with var icella zoster virus, which then remains dormant in the dorsal root ganglia. Reactivation of the virus causes shingles . Chickenpox is usually a mild disease of childhood. An itchy ve sicular rash appears, most densely on the trunk and face, but decreasing peripherally. The lesions appear in crops and crust over in 3 \200\2234 days. Fever, malaise and muscle aches may occur in adults. Infectivity starts 3 days before the rash appears and lasts until the last lesion has crusted. Treat symptomatically, eg calamine lotion for itching and paracetamol for fever. Occasional ly, antibiotics are needed for secondary bacterial skin infection (usually Staph . or Strep .). Pneumonia is rare and in children is usually staphylococcal, but in adults may be caus ed by chickenpox virus. Chickenpox may be severe in neonates and in patients with cystic \201 brosis or immune de \201 ciency, who need specialist assessment and treatment with ac iclovir and/or varicella-zoster immune globulin. Consider aciclovir also for adults and old er adolescents (see BNF ). Shingles often occurs in the elderly and may affect any dermatom e, most often thoracic. The pain of shingles may cause diagnostic dif \201 culty until the rash appears, usually after 1 \200\2234 days. Erythema is followed by vesicles and then cr usting of lesions in a unilateral distribution over 1 dermatome or 2 adjacent dermatomes. O phthalmic shingles may affect the eye via the long ciliary nerves: skin lesions on the side of the tip of the nose imply a high risk of eye involvement. Oral lesions occur in maxilla ry and mandibular shingles. Infection of the geniculate ganglion causes a facial palsy with lesions in the pinna of the ear and on the side of the tongue and hard palate (Ramsay \200 \223Hunt syndrome ). In severe shingles there may be weakness of muscles supplied by nerves of the same spinal root. Antiviral treatment (aciclovir, famciclovir, or valaciclovir) d r isk of post-herpetic pain if given early (within 72hr of start of rash). Dose : aciclovir 8 00mg 5 times daily for 7 days. In renal failure antiviral drugs may cause severe toxicity, so use much smaller or less frequent doses. Patients with immune de \201 ciency or ophthal mic zoster need immediate specialist referral and antiviral treatment. Give analgesia. Anti biotics may be required for secondary infection. Herpes simplex Primary herpes simplex infection causes painful vesicles and ulceration of t he mouth or genitalia ( b p.238). The virus may be inoculated into skin by trauma (herpes g ladiatorum, scrumpox) or by contamination of \201 ngers causing herpetic paronychia (whit low). Infection of the cornea may cause dendritic ulcers ( b p.543). Herpes simplex meningi tis and encephalitis ND are uncommon, but may be fatal, especially in immunode \201 cient patients. The herpes simplex virus persists in sensory ganglia and may be reactivated by st imuli such as sun, cold, trauma, or viral infections. Recurrence of cold sores of the lips is often preceded by tingling: aciclovir cream or tablets may prevent the development of ve sicles. Secondary bacterial infection may require antibiotics. Do not incise a suspected wh itlow. Cover it with a dressing and advise care to avoid spreading infection to the lips or eyes. 241 INFECTIOUS MONONUCLEOSIS (GLANDULAR FEVER) Infectious mononucleosis (glandular fever) Infection with the Epstein \200\223Barr virus is common in children and young adults and is spread by saliva or droplets. Infection often o ccurs without clinical disease. In glandular fever there is malaise, fever, a sore throat, and cervical lymphadenopathy. The throat may be very red and in 25 % of cases there is also infection with a B -haemolytic streptococcus. In severe cases there is marked oedema of th e throat with tonsillar swelling and a membranous exudate ( \200\230anginose \200\231 infec tious mononucleosis) with dif \201 culty in swallowing and breathing. A rash is uncommon u nless ampicillin or amoxicillin are given, causing a widespread erythematous maculopapular rash (which does not signify allergy to penicillins in general). Complications of infectious mononucleosis include respiratory obstruction, ruptured spleen (spontaneously or after minor trauma), thrombocytopenia, jaundice, meningitis, encephalitis , facial palsy, and acute polyneuritis (occasionally causing respiratory failure). Investigations FBC and blood \201 lm (for atypical lymphocytes), Monospot test or Paul \200\223Bunnell test (which may be \200\223ve initially). Differential diagnosis includes cytomegalovirus and toxoplasmosis. Treatment is unnecessary in most patients. Severe or complicated cases need specialist asse ssment and follow-up. In anginose infectious mono- nucleosis, a short course of high dose o ral steroids gives rapid relief of symptoms (prednisolone 80mg on day 1; 15mg tds on days 2 \200\2233; 10mg tds on days 4 \200\2235; 5mg tds on days 6 \200\2237). Steroids are also h elpful in patients with neurological complications. Concurrent B -haemolytic streptococcal infection requires erythromycin (500mg qds), which would also treat the rare unrecognized c ase of diphtheria. 242 CHAPTER 5 Infectious diseases Human immunode \201 ciency virus (HIV) First reports of acquired immune de \201 ciency sy ndrome (AIDS) involved homosexuals in the USA in 1981. HIV (previously called HTLV-III, LAV , or ARV) was identi \201 ed as the causative agent in Paris in 1983. Structure and pathogenesis HIV is an RNA retrovirus. Retroviruses are characterized by havi ng the enzyme reverse transcriptase. This allows viral RNA to be transcribed (copied) into DNA and incorporated into host cells, which then make a new virus. This mechanism has prove d dif \201 cult to overcome: no \200\230cure \200\231 or \200\230vaccine \200\231 is yet available. Glycoproteins on the surface of HIV bind to speci \201 c receptors on target cells. The ce llular receptor for HIV is the CD4 molecule. CD4 receptors are found on a variety of cells, particularly helper/inducer T lymphocytes ( \200\230CD4 cells \200\231), but also monocyte s and macrophages. CD4 cells normally play a crucial role in co-ordinating the immune respo nse: as HIV infection progresses and CD4 cell counts d , the patient develops profound cell ular immunode \201 ciency. Although other complex mechanisms are also involved, CD4 cell c ounts provide a useful index of disease stage and progress. Transmission HIV has been found in many body \202 uids, but is mostly transmitted via blo od, semen, cervical secretions and, perhaps, breast milk. It may be acquired by: \200 Sex ual intercourse (vaginal or anal), with i risk of transmission where individuals already ha ve a genital mucosal breach (eg co-existent STD). Risk of transmission from HIV + ve pregnant mother to baby is 8 15 % . \200 Transfusion o f unscreened blood/blood products (screening started in 1985 in the UK). Contaminated needles shared amongst IV drug abusers. Needlestick injuries from an HIV positive source carry a risk of 8 0.3 % . Diagnosis and HIV testing Antibodies to HIV provide evidence of infection and form the basi s of current blood tests, but these antibodies may not appear until 3 months after exposure . HIV testing is not appropriate in the ED, but reserved for clinics where informed consent and counseling are available. Refer patients requesting HIV tests to local Infectious Dise ases/GU clinics or advisory organizations, eg Terrence Higgins Trust (tel. 0808 802 1221), or the NHS Sexual Health Helpline (24hr freephone 0800 567 123). Natural history of HIV infection HIV infection progresses through phases, which form the ba sis of the two commonly used classi \201 cation systems (World Health Organization (WHO) a nd CDC systems). Acute infection is often sub-clinical, but 2 \200\2236 weeks after exposure there may be a non-speci \201 c febrile illness with lethargy, myalgia, sore throat, lymphadenopathy, and often a maculopapular rash on the face and trunk. This illness usually resolves after 1 \200\2232 weeks but sometimes persists for longer. A long asymptomatic period ( 8 10 years) follows the initial illness. 243 HUMAN IMMUNODEFICIENCY VIRUS (HIV) Some patients develop persistent generalized lymphadenopathy (PGL), with lymphadenopathy ( > 1cm) at two non-inguinal sites for 3 months. Patients become symptomatic as their immunit y d , developing unusual infections and tumors. Many are \200\230AIDS-de \201 ning diseas es \200\231 (see below). The label \200\230AIDS \200\231 has signi \201 cant psychologica l connotations. Most patients with AIDS survive > 2 years. Anti-retroviral drugs (AZT and other drugs) delay the onset of AIDS in asymptomatic patient s and i length of survival. \200\230HAART \200\231 (highly active antiretroviral therapy) is a regime combining 3 or more anti-HIV drugs. Initial presentation of HIV to the emergency department Many HIV + ve patients attending th e ED are aware of their HIV status. Some patients, however, present with HIV-related illnes s, without knowing (or admitting) that they are HIV + ve. Presentation of any of the diseas es listed below should arouse particular suspicion. Centers for Disease Control classi \201 cation of HIV infection Group I Acute infection Gr oup II Asymptomatic Group III Persistent generalized lymphadenopathy Group IV Symptomatic i nfection with subgroups: A \200\224 constitutional disease (fever, diarrhea, weight loss) B \200\224 neurological disease (dementia, peripheral neuropathy) C \200\224 secondary infectious diseases D \200 \224 secondary cancers (lymphomas, Kaposi \200\231s sarcoma) E \200\224 other conditions Some AIDS-de \201 ning diseases in HIV + ve patients \200 Pneumocystis jiroveci pneumoni a (previously called P. carinii ). \200 Kaposi \200\231s sarcoma. \200 Tracheobronchial or oesophageal candidiasis. \200 Cerebral toxoplasmosis. \200 Pulmonary TB. \200 Cyt omegalovirus retinitis. \200 Cerebral lymphoma. \200 Recurrent Salmonella septicaemia. \200 Disseminated histoplasmosis. \200 Invasive cervical carcinoma. \200 Disseminated coccidioidomycosis. \200 Cryptococcosis. \200 Cryptosporidiosis. \200 Progressive mu ltifocal leucoencephalopathy. \200 Oesophageal or bronchial herpes simplex. CD4 counts and AIDS CD4 counts provide an indication of disease progession: many HIV + ve p atients know what their last count was. In the USA, CD4 counts <200/mm 3 may also be used t o de \201 ne AIDS. 244 CHAPTER 5 Infectious diseases Presentation of HIV + ve patients Many patients with symptomatic HIV infection bypass the E D and liaise directly with the specialist unit caring for them. Assessment of HIV + ve pati ents is dif \201 cult in the ED, where advanced infections may present with relatively few signs and little past history is available. Similarly, interpreta- tion of investigations is dif \201 cult without knowledge of previous results. It is therefore reasonable to have a low threshold for specialist referral. HIV + ve patients may present with a variety of c omplications: Respiratory problems As CD4 counts d , pneumonia due to Pneumocystis jiroveci (previously P neumocystis cariniii ) becomes more likely and it is a common indicator diagnosis of AIDS. A non-productive cough occurs with dyspnoea and fever. CXR may show bilateral interstitial mid-zone shadowing, but may be normal. Obtain blood and sputum cultures, rehydrate with IV \202 uids as necessary and refer urgently for IV co-trimoxazole or pentamidine steroid s. Occasionally, Pneumocystis infection may present with fulminant respiratory failure need ing emergency tracheal intubation and IPPV. Other common infections include Aspergillus , C ryptococcus and TB. Injecting drug users are at increased risk of bacterial infection, espe cially Haemophilus in \202 uenzae and Strep. pneumoniae . Neurological problems Cryptococcus neoformans meningitis may present with headache, fever a nd sometimes d conscious level. Neck stiffness and photophobia are rare. Obtain a CT scan t o exclude space-occupying lesions before LP and CSF examination. Cerebral toxoplasmosis may present similarly, often with focal signs or \201 ts. Neurological problems may also be caused by cerebral lymphoma, progressive leucoencephalopathy (focal de \201 cits secondary to papovaviruses), CMV encephalitis (retinopathy is usually present \200\224 see below) a nd HIV-associated delirium or dementia. Eye problems The most signi \201 cant eye problem is Cytomegalovirus (CMV) retinitis , occ urring in 15 % of patients. This presents with blurred vision, blind spots, \200\230 \202 oaters \200\231 or \202 ashing lights, and d VA. Characteristic retinal changes are irre gular yellow-white lesions and perivascular hemorrhages that have been called \200\230pizz a pie \200\231. Retinal detachment may occur. Refer urgently for ophthalmological assessmen t and treatment with ganciclovir or foscarnet. Mucocutaneous problems Oral candidiasis, seborrhoeic dermatitis, and oral hairy leukoplakia (white ridges on lateral border of tongue) are often seen before AIDS develops. As immunit y d , patients may develop herpes simplex, herpes zoster and molluscum contagiosum. Gum ble eding and dental problems are common: the former may be due to thrombocytopenia. Kaposi \200\231s sarcoma is seen in skin and mucous membranes, particularly in homosexuals with AI DS. It is rarely life-threatening, but requires specialist evaluation and treatment. 245 PRESENTATION OF HIV +VE PATIENTS Gastrointestinal problems Nausea, vomiting, diarrhea and weight loss are common complaints and can be due to drug therapy. Dysphagia may result from oesopha- geal candidiasis, herpes simplex, CMV, or Kaposi \200\231s sarcoma, all of which require specialist investigation a nd treatment. CMV colitis can cause a serious illness, characterized by abdominal pain, diarrhea and feve r. Obtain plain X-rays if the recognized complication of toxic dilatation is suspected. Oth er frequently implicated infective causes of diarrhea include cryptosporidium, Giardia , mi crosporidium and Salmonella . Send stool specimens (including for Clostridium dif \201 cil e ) and treat severe diarrhea by IV rehydration and correction of electrolyte imbalance bef ore referral. Hepatitis viruses are likely to complicate the picture in injecting drug users, many of who m are infected with hepatitis B and C. Drug reactions and side effects Many patients will present with symptoms due to drug therap y. This may not be initially apparent: the safest approach is to exclude tumors and opportu nistic infection \201 rst. HIV and emergency department staff ED staff are often concerned about the possibility of ac quiring HIV from patients. The need to perform invasive emergency procedures on \200\230hi gh risk \200\231 patients makes these concerns understandable. Additionally, apparently \200\230low risk \200\231 patients may also pose a threat. Therefore treat every patient as if he is \200\230high risk \200\231. The risk to ED staff is largely in the form of needl estick injury (although the risk of acquiring HIV following needle- stick from a HIV + ve s ource can be d by post-exposure prophylaxis \200\224 see b p.418). Safe practice is re \202 ected in the recommended standard pre- cautions (see b p.32) \200\224 follow these in all patients. Pregnant staff should not treat patients with AIDS (because of concern about CMV and herpes simplex virus). Handling HIV + ve patients Despite vigorous attempts to educate the general public, HIV and AIDS remain taboo subjects amongst many in society. It is imperative to treat all patients , including those who are HIV + ve, with sensitivity and compas- sion. Touching and shaking hands with HIV + ve patients is perfectly safe, and may help to reassure them that the dis crimination and irrational treat- ment they may have received outside hospital does not ext end into the ED. In view of prevailing attitudes towards HIV, patient con \201 dentiality is of the utmost importance. Remember that family and friends accompanying the patient may be unaware of his HIV status. HIV + ve staff The risk to patients from ED staff infected with HIV is minimal, but remains a theoretical possibility. Staff who believe that they may be HIV + ve must obtain and fol low occupational health advice. Needlestick injury: See b p.418. 246 CHAPTER 5 Infectious diseases Imported infectious diseases Patients may present to the ED with infectious diseases acquir ed abroad. It is essential to ask where a patient has been, especially in the 6 weeks befor e the onset of symptoms. The most common imported diseases are bowel infections causing dia rrhea ( b p.226). Less common, but very important diseases include malaria ( b p.247), typh oid ( b p.248), Legionnaires \200\231 disease ( b p.110) and hepatitis ( b p.239). Rabies ( b p.249) and viral haemorrhagic fevers, such as Lassa fever ( b p.250) are very rare in th e UK. Occasionally, tropical diseases are acquired in Britain from bites by infected insects carr ied by plane (eg \200\230airport malaria \200\231). Advice about tropical diseases is available from departments of Infectious Diseases or Trop ical Medicine: \200 Birmingham (Heartlands Hospital). www.heartofengland.nhs.uk Telephone 0121 424 2000. Liverpool (School of Tropical Medicine). www.liv.ac.uk/lstm Telephone 0151 705 3100. London (Hospital for Tropical Diseases) www.thehtd.org/Emergencies. aspx Telephone 0845 155 5000. Oxford (Churchill Hospital) Telephone 01865 741 841. \200 Glasgow (Brownlee Center for In fectious and Communicable Diseases, Gartnavel General Hospital) Telephone 0141 211 3000. A public access website provided by the NHS which gives information for people traveling ab road from the UK is www. \201 tfortravel.scot. nhs.uk Pyrexia of unknown origin in travelers Think of and check for malaria ( b p.247) in any feb rile patient who has been in a malarious area. Consider Lassa fever ( b p.250) in someone w ho has been in West Africa in the previous 3 weeks. Typhoid ( b p.248) often presents as a septicaemic illness with constipation, rather than diarrhea. TB ( b p.232) and brucellosis may cause fever and sweating at night. Investigations (warn lab of possible risks) FBC, thi ck and thin blood \201 lms for malaria, U&E, blood glucose, blood culture, urine stick te sting, microscopy and culture, CXR. Further investigations may include LFTs and viral titres. Management Barrier nurse in a cubicle (use a negative pressure room if available). Wear gow n, gloves, goggles and mask. Record vaccination and prophylaxis history, with countries and areas visited, and dates of travel and onset of symptoms. Look particularly for confusion, dehydration, jaundice, rashes, chest signs, liver and spleen enlargement and tenderness, l ymphadenopathy, neck stiffness, photophobia. Seek expert advice at once if the patient is v ery ill or there is concern about typhoid or Lassa fever or other viral haemorrhagic fevers . Refer to an Infectious Diseases specialist. 247 MALARIAND Malaria ND Malaria is very common in the tropics and subtropical regions, and is a parasiti c infection transmitted by mosquitoes. The \201 ve species which cause malaria in humans are Plasmodium falciparum, P. vivax, P. malariae, P. ovale, and P. knowlesi. Falciparum ( \200\230malignant tertian \200\231) malaria is the most important, since it may be rapidly fatal and drug-resistant strains are common. Serious complications are unusual in the other types of malaria, but they may cause febrile convulsions in children. In the UK malaria oc curs in travelers from malarious areas, especially P. vivax from the Indian subcontinent an d P. falciparum from Africa, South- East Asia, and Central and South America. Malaria often develops despite antimalarial tablets, because of drug resistance or incorrect dosage. Che ck for malaria in any febrile illness within 2 months of visiting a malarious area. Common misdiagnoses are in \202 uenza and viral hepatitis. Clinical features The incubation period is usually 7 \200\22314 days for P. falciparum and 12 \200\22340 days for other types of malaria, but occasionally it is much longer ( > 1 yea r), especially in P. malariae and P. vivax infections. There is malaise, fatigue, fever and head- ache followed by paroxysms lasting 8 \200\22312hr of rigors, vomiting and then sever e sweating. The fever may be periodic (classically 48hr in P. ovale or P. vivax, and 72hr i n P. malariae ). Haemolytic anemia, jaundice and splenomegaly may occur, but lymphadenopath y is not a feature. P. falciparum may cause cerebral malaria with coma, \201 ts and focal neurological signs. Diarrhea, cardiac failure, pulmonary oedema and shock may occur. Deter ioration can be rapid. Investigations Consider Lassa fever ( b p.250) in recent visitors to West Africa. In any ill patient who has been in a malarious area send blood for thin and t hick \201 lm examination for malaria. Repeated blood \201 lms may be needed. Also arran ge FBC (since malaria may cause anemia, thrombocytopenia and neutropenia), blood glucose (h ypoglycaemia may be severe), U&E (renal failure is possible), and test the urine for blood ( \200\230black water fever \200\231). Treatment of falciparum malaria 1 Careful monitoring is needed ICU. Obtain expert advice from a tropical disease specialist ( b p.246), espe cially if the patient is severely ill or has come from south-east Asia, where there is wide spread drug resistance. Give quinine, orally or IV depending on the severity of illness: or al quinine sulfate 600mg (adult) or 10mg/kg (child) every 8hr for 7 days, followed by doxyc ycline 200mg od for 7 days, clindamycin 450mg tds for 5 days or Fansidar 3 tablets. Alte rnative oral drugs are Malarone (proguanil with atovaquone) or Riamet (artemether wit h lumefantrine): for details see BNF. For algorithm 1 see www.britishinfectionsociety.org . Treatment of benign malarias ( P. vivax, ovale, malariae ) 1 The usual treatment is chloro quine (see BNF ). A course of primaquine is also needed to prevent relapse in vivax and ova le infections, but glucose- 6-phosphate dehydrogenase levels should be checked before prima quine is used, since it may cause haemolysis in G6PD de \201 cient patients. In the UK ref er to an Infectious Diseases unit for treatment and follow-up. 1 Lalloo DG et al . ( 2007 ) UK malaria treatment guidelines . Journal of Infection 54 : 11 1 \200\223 121 . 248 CHAPTER 5 Infectious diseases Typhoid ND and paratyphoid ND (enteric fever) These fevers, caused by Salmonella typhi and S. paratyphi A, B, or C, occur throughout the world, especially where hygiene is inadequate . They are spread by contamination of food or water by urine or feces from a patient or an asymptomatic carrier. Typhoid may occur despite immu- nization. Typhoid and malaria are the \201 rst diseases to consider if fever develops soon after a visit to the tropics. The i ncubation period is usually 7 \200\22314 days, but may range from 3 \200\22360 days. Initial symptoms Headache, fever, and a dry cough, with abdominal discomfort and anorexia. Constipation is common, but diarrhea may occur, especially in children. Confusion and hallu cinations may develop. Physical examination This may be normal except for fever. There may be a relative brady- ca rdia (ie less than the usual 15 beats/min i in pulse rate per C of fever). Splenomegaly and abdominal tenderness occur, but there is no lymphadenopathy. \200\230Rose spots \200 \231 are pink macular spots on the lower chest or upper abdomen which blanch on pressure. T here may be signs of pneumonia or dehydration. Intestinal perforation or hemorrhage occur o ccasionally. Investigations FBC (mild anemia is common, WBC usually normal), blood \201 lms for malari a, U&E, LFTs, blood cultures, CXR (for signs of TB or pneumonia). Treatment Isolate and barrier nurse. Admit suspected cases to an Infectious Diseases unit a nd notify the local consultant in Communicable Disease Control. The usual drug treatment is with cipro \202 oxacin or cefotaxime but other antibiotics may be needed for drug-resista nt infections. Dengue Dengue is a mosquito-borne viral infection which is common in southern Asia, the wes tern Paci \201 c, central Africa and central and south America. Most infections are asympt omatic. Symptoms start after an incubation period of 4 \200\2237 days with fever, malaise, nausea and vomiting, headache, severe muscle and bone pains ( \200\230break bone fever \200 \231). Some patients have a transient macular rash, petechiae, lymphadenopathy, hepatomegal y, d WCC and platelets and i liver enzymes. Most patients recover after 3 \200\2237 days wi th symptomatic treatment. A few develop dengue shock syndrome (DSS) with hypotension, pleur al effusions, ascites, d plasma protein and bleeding problems. Abdominal pain may be severe . Treatment is supportive, with careful \202 uid balance management and IV \202 uids in DSS. With expert care most patients with severe dengue eventually make a full recovery. 249 RABIESND Poliomyelitis ND Paralytic poliomyelitis is rare in developed countries where vaccination i s routine. Fever is followed by signs of meningitis, pain and spasm in limb muscles. Respir atory failure may be fatal. Resuscitate and ventilate if necessary and refer to ICU. The differential diagnosis include s Guillain \200\223Barr syndrome ( b p.142) and organophosphate poisoning ( b p.206). Rabies ND Rabies is a viral infection of mammals that occurs in most parts of the world, in cluding much of the Arctic, as well as tropical and temperate regions. At present it is not endemic in the UK, Norway, Sweden, Iceland, Australasia, or Japan. Human and animal rabies is most common in the Indian subcontinent, China, Thailand, the Philippines, and parts of South America. Most human infections result from dog bites, but rabies can be transmitted b y many other domesticated or wild animals, such as cats and foxes. Rabies virus in an anima l \200\231s saliva may cause infection by contamina- tion of a bite or scratch or by absorp tion through mucous membranes of the eye, mouth or nose. Rarely, infection occurs from inha lation of the virus in bat-infested caves. Prevention of rabies after a bite is described o n b p.415. Advice about post-exposure treatment and suspected cases of rabies is available in the UK from the Health Protection Agency. For details see www.hpa.org.uk/Topics/Infectio usDiseases/InfectionsAZ/Rabies Clinical features The incubation period of rabies is usually 3 \200\22312 weeks, but can va ry from a few days to > 2 years. The \201 rst symptoms are itching, tingling or pain at the site of the bite wound. Headac he, fever, and malaise occur, with spreading paralysis and episodes of confusion, hallucina tion and agitation. Hydrophobia is characteristic: attempts at drinking cause spasm of musc les involved in breathing and swallowing and also profound terror. In 8 20 % of cases there is \200\230dumb rabies \200\231 with increasing paralysis but no episodes of spasm or hyp eractivity. Rabies is almost always fatal, even with ICU treatment. Management If rabies is suspected, barrier nurse the patient in a quiet room with the minim um of staff, who must wear gowns, gloves, eye protection and masks. Obtain advice immediate ly from a specialist in Infectious Diseases. Anticipate press enquiries. Record the names o f all staff involved, so that they can be offered rabies immunization. 250 CHAPTER 5 Infectious diseases Viral haemorrhagic fevers ND Lassa fever Lassa fever occurs in many rural parts of West Afr ica. It is a viral infection acquired from infected blood or secretions, transmitted by ina dvertent innoculation (eg needlestick injuries) or contamination of mucous mem- branes or b roken skin. In Africa it is transmitted by multimammate rats. The incubation period is up t o 3 weeks. There is a high mortality.