The infectious diseases/tropical medicine placement is an excellent opportunity to see a wide variety of presentations and exotic diseases; patients will have various stories and different systemic involvement. Your overall medical skills such as history taking (especially the travel history), clinical examination, and diagnostic skills will be vital throughout this placement and will be developed further.
On the wards
You could see anything from skin and soft tissue infections such as cellulitis, and necrotizing fasciitis to more deep-seated infections such as septic arthritis, osteomyelitis, meningitis, encephalitis, and infective endocarditis (covered elsewhere in the book).
You will get the opportunity to meet patients from various ethnicities and social backgrounds, each with a different story and illness. Patients that come to mind include the migrant labourer with reactivation of TB, the keen hiker who caught Lyme disease from trekking in the New Forest, and the farmer who developed Q-fever during the lambing season.
In the ED
You will meet others with exciting travel histories, some will present with a simple diarrhoeal illness, others with potentially life-threatening infections such as malaria.
Overall, in infectious diseases you will see very ill people improve dramatically following your intervention. Your expertise will not be limited to one system or organ, which keeps things fresh. You will also work closely with various specialties, as well as public health agencies and community teams to improve patient outcomes and prevent outbreaks.
In the UK, malaria is a serious imported infection caused by single-celled parasites from the Plasmodium species. Transmitted by the female Anopheles mosquito, it is a medical emergency and prompt diagnosis and management is vital. Globally, malaria continues to be a major issue. Figures released by the WHO estimate the burden was over 200 million cases worldwide, with nearly half a million deaths in 2015. Most of these cases were in sub-Saharan Africa and South-East Asia. In 2016, there were 1618 reported malaria cases in the UK (real numbers are probably double that) with six deaths/year over the past decade. There are five Plasmodium species where 80% of infections in the UK are due to P. falciparum. Species include:
• P. falciparum
• P. vivax
• P. ovale
• P. malariae
• P. knowlesi.
Documented as an illness for >4000 years; the name probably originates from the Italian word Mal’aria meaning ‘bad air’. It was not until 1880 that the malaria parasites were discovered and since have been studied extensively and treated. (See Fig. 20.1.)
Patients are returning travellers from endemic areas who often present with fever, rigors, sweats, and malaise; but it could also present with non-specific symptoms such as headaches, myalgia, diarrhoea, and cough. The symptoms can occur anywhere from 6 days to 3 months following exposure in cases of P. falciparum. However, P. ovale and P. vivax can present months or (rarely) years later, especially if treated in the past, as these two can present following auto-infection with the dormant liver stage of the parasite (hypnozoite). You will need to take a thorough travel history, noting country and area of travel, including stop-overs, and date of return to the UK. Do not forget to ask about malaria prophylaxis, i.e. the name of drug, dosage, and adherence.
Once malaria is suspected, thick and thin blood films for microscopy should be sent to the haematology lab urgently. This is in addition to a FBC, U&E, LFTs, clotting, and blood gas analysis including lactate and glucose. If the first sample is negative but the clinical suspicion remains, further samples should be sent 12–24 hours later. If three films are negative, malaria is unlikely. Clinical assessment and systemic examination will exclude severe malaria or concurrent infections.
• Impaired consciousness or seizures.
• Renal impairment (oliguria <0.4 mL/kg/hour or creatinine >265 mmol/L).
• Acidosis (pH <7.3).
• Hypoglycaemia (<2.2 mmol/L).
• Pulmonary oedema or ARDS.
• Hb ≤8 g/dL.
• Spontaneous bleeding/DIC
• Shock (algid malaria—BP <90/60 mmHg).
• Haemoglobinuria (without G6PD deficiency).
• Parasitaemia >10%.
Uncomplicated falciparum malaria
There are three therapeutic options for the treatment of uncomplicated falciparum malaria. Artemisinin combination therapy (ACT, e.g. Riamet® or Eurartesim®) is the preferred option as they are more effective against the parasite throughout its life cycle. However, if ACT is not available, atovaquone–proguanil (Malarone®), and oral quinine sulfate + doxycycline are other available options.
Complicated falciparum malaria
Parenteral therapy is the mainstay treatment of complicated falciparum malaria. Parenteral therapy should also be considered in cases of parasitaemia >2% and pregnant women with artesunate (IV for 1–5 days followed by a full course of an oral ACT) or quinine dihydrochloride (IV followed by a course of quinine + doxycycline/clindamycin).
Either an oral ACT or chloroquine can be used to treat the blood forms of all non-falciparum species. In cases of P. vivax and P. ovale, the treatment regimen should include primaquine to eliminate the dormant liver stage (hypnozoite) to prevent relapse. Test patients for G6PD deficiency before treatment with primaquine.
Viral haemorrhagic fevers
You have probably heard of the recent devastating outbreak of Ebola in West Africa. Patients are returning travellers from endemic areas who present with non-specific symptoms such as fever, malaise, vomiting and diarrhoea. Patients could present with bruising or active bleeding (hence the haemorrhagic in viral haemorrhagic fevers). It is important to be aware of current outbreaks which you could find on Public Health England’s website ( www.gov.uk/guidance/viral-haemorrhagic-fevers-origins-reservoirs-transmission-and-guidelines). Patients present within 3 weeks of returning from an endemic area but malaria needs to be excluded first! Patients will require specific infection control precautions including patient isolation according to local policies as well as special sample handling by the lab. Treatment for viral haemorrhagic fevers is supportive, focusing on correcting metabolic and electrolyte abnormalities, as well as treating potential concurrent infections and organ support if needed. Viral families include Arenaviridae, Flaviviridae, Bunyaviridae, Filoviridae.
Caused by the single-celled (protozoan) parasite Entamoeba histolytica in ~10 % of the world population. It is transmitted via the faeco-oral route so ask about eating habits, as well as water sources for drinking, ice, cooking, and brushing teeth! Symptoms: vary from asymptomatic to the commoner diarrhoeal illness; however, amoebiasis could cause dysentery and colitis in severe cases. Extraintestinal amoebiasis can occur if the parasite spreads beyond the intestine, and causes an amoebic liver abscess RUQ pain and fever. Diagnosis requires imaging of the abdomen (e.g. US scan), stool MC&S, or aspiration (dark red-brown colour described as ‘anchovy paste’). Treatment: pharmacotherapy and an interventional assessment in cases of severe colitis and liver abscess. Paromomycin, iodoquinol, and diloxanide furoate are luminal agents (minimal GI absorption) that can be used for asymptomatic or mild infections. Metronidazole is reserved for severe disease.
Soil-transmitted helminth infections
Affects ~1.5 billion people worldwide, mostly children. The infection is prevalent in areas of poor sanitation. Transmitted via the faeco-oral route by the ingestion of eggs present in contaminated soil, water, and vegetation. There are three main species that infect humans:
• Roundworm (Ascaris lumbricoides).
• Whipworm (Trichuris trichiura).
• Hookworms (Necator americanus and Ancylostoma duodenale) could also be transmitted by walking barefoot on contaminated soil, as larvae can penetrate the skin.
Mostly asymptomatic but could cause abdominal pain and diarrhoea. Chronic infection could nutritional deficiencies and anaemia. Diagnosed by microscopy of stool samples. Treatment is with albendazole or mebendazole.
Is a parasitic worm infection of the blood trematode (fluke) class. It is estimated that 200 million people worldwide are infected. The infection is transmitted through swimming in contaminated water in endemic areas. Free swimming larvae (cercariae) are released by the intermediate host (fresh water snails) and penetrate the human skin. This causes a pruritic rash, known otherwise as the ‘swimmer’s itch’. The larvae then migrate through the lungs or the liver to their final organ. Depending on species, the adult worm could settle in either the venous plexus of the urinary bladder (Schistosoma haematobium) or the portal venous system (S. japonicum, S. mansoni), and lay their eggs which in turn are released through urine and faeces. The eggs hatch in fresh water and penetrate the snail, continuing the infection cycle. In the travel history, it is important to ask about leisure activities especially swimming and rafting in fresh water. The stereotypical location to contract the infection is Lake Malawi in Africa (prime destination for medical students on electives). Schistosomiasis can cause a myriad of systemic syndromes including acute schistosomiasis (Katayama fever), intestinal, urinary, hepatic, CNS, and chronic schistosomiasis:
• Acute schistosomiasis (Katayama fever) presents within 2 months of infection with fever, headache, hepatosplenomegaly, lymphadenopathy, and peripheral eosinophilia.
• Urinary schistosomiasis (S. haematobium) presents with terminal haematuria, if untreated urinary obstruction or in some cases bladder cancer due to chronic granulomatous inflammation.
The diagnosis is confirmed by detection of eggs in urine or faeces, serological tests are also helpful. Treatment is with praziquantel.
Is the commonest travel-related illness worldwide. ~90% of cases are caused by bacteria; enterotoxigenic Escherichia coli is commonest, followed by Campylobacter, Shigella, and Salmonella species. Viruses such as norovirus, rotavirus, and astrovirus cause ~5–8% of cases. Rarely, traveller’s diarrhoea is caused by parasites such as Giardia and Entamoeba species. Spread is via the faeco-oral route, and depending on the organism, symptoms could start hours to days after ingestion of contaminated food or drink. Symptoms range from mild abdominal discomfort and nausea to vomiting and frequent diarrhoea which could contain blood and mucous (dysentery). Diagnosis is often presumptive if mild, but could be made by microscopy and culture of stool samples if moderate or severe. Treatment is mostly supportive for mild cases, using oral rehydration solutions and antimotility agents (not to be used in bloody diarrhoea or patients presenting with fever). Antibiotics (e.g. azithromycin or fluoroquinolones) are reserved for moderate to severe cases.
Is caused by a flavivirus, endemic in the tropics, and transmitted by the Aedes mosquito. Symptoms start within 2 weeks of infection and include fever, headache, retro-orbital pain, myalgia, and a maculopapular rash. In cases of repeated infection, patients can present with confusion, petechiae, bruising, and signs of shock due to hypovolaemia and coagulopathy (Dengue shock syndrome). Diagnosis is often made by serology (raised Dengue IgM in acute infection) or detection by PCR. Treatment is supportive with antipyretics, rehydration, and circulatory support in severe cases. The Chikungunya virus is an alphavirus, also transmitted by the Aedes mosquito, and therefore endemic in the same areas as Dengue with similar management.
TB most commonly presents as a primary lung infection. However, following the initial infection which could be asymptomatic, Mycobacterium tuberculosis can lie dormant for years to reactivate later in the form of extrapulmonary TB. Profound immunosuppression due to frailty, biologic agent use, cancer chemotherapy, or HIV infection are known risk factors; however, reasons for reactivation in apparently immune competent individuals are poorly understood. The mainstay of diagnosis is biopsy and culturing the organism from tissue or bodily fluid samples, this is often difficult due to the low yield from culturing bodily fluids such as CSF. Detection by PCR could also be used, especially in determining resistance to rifampicin. Interferon-gamma release assays (QuantiFERON-TB Gold®, T-SPOT®.TB) are helpful in determining prior exposure to TB, but their sensitivity is reduced in profound immunosuppression. Systemic manifestations include the following:
• TB meningitis (e.g. bacterial meningitis): presents with fever, meningism (headache, neck stiffness, and photophobia), reduced consciousness, and coma. The CSF shows a lymphocytic predominant pleocytosis, with a very high protein level but very low glucose.
• CNS tuberculoma: presents as a space-occupying lesion, symptoms depend on the area of the CNS affected. It is typically formed of a caseating granuloma. Diagnosis is with biopsy and culture.
• TB osteomyelitis: confirmed by culture.
• TB adenopathy: presents with fever, night sweats, and lymphadenopathy. Diagnosis is confirmed by culture/PCR from biopsied lymph node.
• Intraocular TB: rare and presents with reduced vision or pain in cases of TB uveitis. Diagnosis is often presumptive; but the organism can be detected by PCR/culture from aqueous/vitreous samples.
Treatment is similar to pulmonary TB initially, with a 2-month induction phase with quadruple therapy (rifampicin, isoniazid, ethambutol, and pyrazinamide + pyridoxine to prevent isoniazid-induced peripheral neuropathy). This is followed by a consolidation phase with rifampicin, isoniazid, and pyridoxine for the remainder of the course. The total duration depends on the location. CNS involvement requires a total of 9–12 months of treatment, others usually require at least 6 months. Investigation of the immune status is vital (i.e. HIV testing).
Is a widely-disseminated herpes virus that spreads by intimate contact with body fluids, primarily saliva, from asymptomatic carriers or infected patients. The virus remains latent in most infected cells and can be reactivated after the acute phase. Most of the EBV infections are subclinical. Infectious mononucleosis/glandular fever/kissing disease is common in adolescence and consists of fever, tonsillitis ± pharyngitis and cervical lymph node enlargement with atypical lymphocytosis preceded by 1–2-week prodromal phase of anorexia and malaise. Lymph node enlargement could be out of proportion producing upper airway obstruction. Pharyngitis (with palatal petechiae in 25–60%), hepatomegaly, splenomegaly, periorbital oedema, and lymphadenopathy are common on examination. Some complications include mild hepatitis (95%), cytopaenias (usually self-limited), splenic rupture, and neurological complications of meningitis, encephalitis, and seizures. Morbilliform rash following the administration of penicillin (possibly immune-mediated) is also a common complication. EBV is associated with a variety of lymphoproliferative disorders and some malignancies such as African Burkitt lymphoma and nasopharyngeal carcinoma. EBV-infected B cells produce monoclonal IgM antibodies (heterophile antibodies) that are measured using various agglutination tests (Paul–Bunnel/monospot test). 90% have developed these antibodies by week 3 and they usually disappear within the first 3 months. EBV-specific antibodies (viral capsid antigen and Epstein–Barr nuclear antigen) confirm acute, late, or past infection. Most cases are self-limited and do not require specific therapy. Steroids may be indicated in cases of severe thrombocytopenia, haemolytic anaemia, impending airway obstruction, and for CNS or cardiac involvement.
Salmonella enterica serotypes Typhi and Paratyphi (A, B, and C) can cause a potentially severe bacteraemic illness referred to as typhoid and paratyphoid fever, respectively. It is acquired by consumption of water or food contaminated by faeces of an acutely infected, convalescent person, or a chronic asymptomatic carrier. Endemic areas include southern Asia (India, Pakistan, Bangladesh), south-east Asia, and Africa. Incubation period 6–30 days. Insidious onset with increasing fatigue and high fever (with relative bradycardia) followed by headache, malaise, anorexia, abdominal pain, and diarrhoea or constipation. Complications include cholecystitis, intestinal haemorrhage, and perforation. Diagnosis with blood cultures (+ve in 50% of patients) or bone marrow (highest yield). Urine and stool samples are positive at a late stage. Quinolones are the drug of choice, but if there is suspicion of resistance (i.e. >80% in most of Asia), ceftriaxone or azithromycin are alternatives. 1% of patients become chronic carriers (will need treatment if at risk of spreading disease, e.g. food handlers). Typhoid vaccine exists just for typhoid fever and is recommended for all travellers to endemic areas. Immunization is not 100% effective.
Is caused by influenza viruses type A, B, and C spread from person to person through respiratory droplets. Subtypes of influenza A are classified based on surface proteins: haemagglutinin and neuraminidase. Distribution of influenza varies every year between geographic areas and time of year. Avian and swine influenza viruses can occasionally infect and cause disease in humans, associated with close exposure to infected animals. Incubation period is 1–4 days. Uncomplicated influenza symptoms include fever, muscle aches, headache, malaise, non-productive cough, sore throat, vomiting, and rhinitis. Complications include primary influenza viral pneumonia, secondary bacterial pneumonia, myocarditis, myositis, and encephalopathy. Adults >65 years, children <2 years, and patients with comorbidities are at higher risk of complications. Diagnostic tests include viral culture, rapid influenza diagnostic tests, immunofluorescence and reverse transcription PCR. The cornerstone of management is an effective vaccination strategy recommended in ‘at-risk’ groups included all patients >65 years, those with diabetes, immunosuppression, and/or with cardiac, lung, or renal disease, and health workers. Early antiviral treatment (<48 hours after onset of symptoms) can shorten the duration of illness and reduce the risk of complications. Oseltamivir (neuraminidase inhibitor) is the preferred agent, recommended in hospitalized patients and patients at higher risk of complications.
Is caused by varicella zoster virus (VZV). Common in childhood and highly contagious (85% secondary attack rates). After primary infection, the virus remains dormant in the sensory nerve ganglia and can reactivate at a later time causing herpes zoster (shingles in 20% of population). Transmission occurs from person to person by inhalation of aerosols from vesicular fluid of skin lesions and infected respiratory tract secretions. The period of transmission begins 1–2 days before the onset of rash and ends when all lesions are crusted. Incubation period 10–21 days. 1–2 days of prodromal symptoms (fever, malaise) usually precedes a pruritic rash consisting of crops of macules, papules, and vesicles that resolve by crusting. The presence of lesions in different stages of development at the same time is characteristic of varicella. Complications are more frequent in infants, adults >65 years, and immunocompromised people and include bacterial skin infection, pneumonia, cerebellar ataxia, meningitis, encephalitis, and haemorrhagic conditions, rarely resulting in death (1/40,000 for children, 15-fold for adults). Diagnosis is usually clinical. Vesicular swabs or scrapings from crusted lesions can be used to identify VZV DNA by PCR (preferred method) or direct fluorescent antibody. Serologic tests are less reliable. Oral/IV aciclovir should be considered in high-risk populations (>65 years, chronic cutaneous or pulmonary disorders, and immunocompromised patients) and in serious complications. Live, attenuated vaccine is recommended in non-immune healthcare workers and close contacts of immunocompromised patients. Its effectiveness is 80% after one dose, 95% after two doses.
Caused by a virus from the genus Morbillivirus and transmitted from person to person by aerosolized droplets. It is highly contagious with an incubation period of 7–21 days. Symptoms include fever, conjunctivitis, rhinitis, and cough followed by small blue-grey spots on an erythematous base on the buccal mucosa (Koplik spots) and a maculopapular rash that usually begins on the face. Infected people are usually contagious from 4 days before until 4 days after rash onset. Common complications include diarrhoea, middle ear infection, and pneumonia. Risk of encephalitis is higher in children <5 years and adults >20 years and in malnourished population. Subacute sclerosis panencephalitis is a chronic, degenerative, neurological complication occurring years after infection. Positive serology test confirms the diagnosis. Treatment is supportive. Vitamin A is recommended for all children with acute measles to reduce the risk of complications. It is preventable with a live, attenuated vaccine given at 1 year and in preschool.
Is produced by poliovirus (genus Enterovirus) which is highly contagious via faecal–oral or oral transmission. Incubation period is 10 days. Most infected patients are asymptomatic and just a minority develop acute flaccid paralysis of a single limb or quadriplegia. Respiratory failure and death are rare. There may be delayed progression or paralysis (post-polio syndrome). Diagnosis requires identifying poliovirus by cell culture or PCR in clinical specimens (usually stools) obtained from an acutely ill patient. Only supportive treatment is available. Prevention includes routine infant immunization by inactivated poliovirus vaccine (IPV) at ages 2, 4, 6–18 months, and 4–6 years. Vaccine confers lifelong immunity. Poliovirus disease is now confined to only two countries: Pakistan and Afghanistan. Adults travelling to these areas who are unvaccinated or whose vaccination status is unknown should receive a series of three doses of IPV.
Is a neurotropic virus from the family Rhabdoviridae transmitted by inoculation of saliva from a bite of a rabid animal (e.g. bats, dogs, cats, and foxes). Symptoms can develop 9–90 days after exposure. Pain and paraesthesia at the site of exposure are often the first symptoms followed by fever, headache, malaise, and rapidly progressing into a fatal, acute encephalitis. It causes 50,000 deaths/year worldwide and is often fatal. Advise travellers to avoid animal contact. If bitten, clean bite wound with soapy water. Pre-exposure prophylaxis is recommended to travellers highly exposed to rabies (e.g. vets, zookeepers, and bat handlers). Treatment if bitten (and previously vaccinated) consists of rabies vaccine on days 0 and 3 after exposure. Post-exposure prophylaxis for an unvaccinated patient consists of rabies immunoglobulin ± vaccine on days 0, 3, 7, and 14. Rabies is a notifiable disease.
Creutzfeldt–Jakob disease (CJD)
Is a human prion disease, classified as a transmissible spongiform encephalopathy (TSE). It is a rapidly progressive, invariably fatal neurodegenerative disorder caused by an abnormal isoform of a cellular glycoprotein known as the prion protein. It occurs in 85% of cases as a sporadic disease. 5–15% develop CJD because of inherited mutations. It presents as a rapidly progressive dementia with myoclonus eventually developing extrapyramidal signs and visual symptoms. Infection usually death within first year of onset of illness. Diagnosis relies on presence of 14-3-3 protein in the CSF and/or a typical EEG pattern (periodic sharp wave complexes). Confirmatory diagnosis requires neuropathological and/or immunodiagnostic testing of brain tissue. No therapy has been shown to stop the progression of this disease and treatment is supportive.
Is produced by tetanospasmin, the exotoxin of Clostridium tetani, transmitted by contact of non-intact skin with contaminated objects. Susceptible wounds include those contaminated with dirt, human or animal excreta or saliva, burns, punctures, or crush injuries. 20% of patients have no evidence of recent wounds. Produces 50 deaths/year in the UK with 40% mortality (80% in neonates). Incubation period 3–10 days. Prodrome of fever, malaise, and headache before classical acute symptoms of muscle rigidity and spasms, often in the jaw (trismus), facial muscles (risus sardonicus), and neck. Progression to generalized tetanus (opisthotonus) may occur respiratory failure and death. There are no confirmatory diagnostic tests available. Treatment includes human tetanus immune globulin (hTIG) to neutralize toxin, agents to control muscle spasm (e.g. diazepam), antimicrobials (first choice metronidazole 500 mg/6 hours), and aggressive wound care included debridement and excision if possible. Prevention includes routine tetanus vaccine: three doses during first year of life and a booster dose during adolescence and early adulthood.
Is caused by the bacteria Borrelia burgdorferi transmitted to humans through the bite of infected blacklegged ticks (Ixodes scapularis). Incubation period 3–30 days. Typical symptoms include fever, headache, fatigue, joint and muscle pains, and a characteristic, painless, annular skin lesion centred on the bite called erythema migrans. 60% of patients do not recall a tick bite. Later features of Lyme disease (weeks to months after the tick bite) can include mono- or polyarthritis (often knee), Bell’s palsy, meningitis, carditis, and severe fatigue. A positive serology test for Borrelia burgdorferi antibodies confirms the diagnosis if added to a suggestive clinical history, they could develop late (90% +ve at 4–6 weeks). CSF serology should be obtained in patients with neurological symptoms. Early-stage manifestations are treated with a course of oral doxycycline or amoxicillin for up to 28 days. If symptoms persist or neurologic symptoms appear, IV ceftriaxone should be considered for 14–30 days.
The returning traveller from the tropics
• It is important to clarify the onset, duration, and progression. Think about incubation periods (see Table 20.1). The pattern of fever is classically described by textbooks for various tropical infections but unlikely to be diagnostically reliable. However, persistent fever at night for months may point towards TB. Is the fever accompanied by drenching sweats?
• Associated symptoms are vital to fish out, especially rigors, described as uncontrolled teeth clattering and shaking, as opposed to goosebumps, chills, or simply feeling hot and cold.
• Go through the systematic review as you would normally. In addition to taking a history of GI, respiratory, and genitourinary symptoms, do not forget to ask about sore throat symptoms, lymphadenopathy, myalgia, arthralgia, and rashes.
Table 20.1 Importance of incubation periods
Short <10 days
Medium 10–21 days
Long >21 days
Amoebic liver abscess
First, you would want to put on your travel agent cap here; you will need to find out the full travel itinerary, including dates of travel, stopovers, locations, and purpose of travel.
Ask about the following:
• Accommodation for the whole trip (hotels vs huts, urban vs rural), food and water sources, do not forget about water used for ice and brushing teeth (food- and water-borne illnesses, e.g. amoebiasis and traveller’s diarrhoea).
• All outdoor activities, especially fresh water activities such as swimming or rafting (schistosomiasis), caving (viral haemorrhagic fevers), and interaction with the locals and animals, if any.
• How good a prevention strategy did they have? Vaccinations, insect repellents, bed nets, and malaria prophylaxis. Ask about drug name, dosage, and compliance. Note that full compliance does not rule out malaria!
• Is anyone else in the group affected?
• Any hospitalizations abroad?
(See Chapter 17.) Taking a comprehensive sexual history is vital in returning travellers—you do not want to miss HIV seroconversion! Ask about the number of partners if any, gender, type of sex, protection, and prophylaxis (pre- or post-exposure prophylaxis).
• General examination: rule out sepsis (capillary refill time, BP, HR, and temperature), look for rashes, bruises, petechiae, and lymphadenopathy.
• Systemic examination: looking for respiratory signs and hepatosplenomegaly; do not forget to examine the throat!
• You will find that the central dogma in infectious diseases is nailing a microbiological diagnosis by sending samples for microscopy, culture, serology, and PCR (choose wisely).
• However, in cases of returning travellers from the tropics with fever:
1. Rule out malaria.
2. Rule out malaria.
3. Rule out malaria.
• In addition to regular blood tests as mentioned in the malaria section (see p. [link]).