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Tropical infectious diseases
Essentials
- 1
Tropical diseases are a major cause of morbidity and mortality worldwide.
- 2
Due to climate change and increasing population mobility (migration and travel), health practitioners in non-tropical areas will increasingly have to diagnose and treat tropical diseases.
- 3
A significant proportion of northern Australia has a tropical climate and several tropical diseases occur in this area. Vigilant public health surveillance, case tracking and vector control are instrumental in controlling incursions of non-endemic tropical diseases into Australia.
- 4
Indigenous Australians are disproportionally affected by infections in tropical Australia.
- 5
Within tropical areas, the aetiological spectrum of common diseases is different from that in temperate areas. This is due to different local prevalences of common pathogens, as well as the existence of specific tropical agents. Knowledge of local protocols is important in choosing appropriate antibiotic cover for the treatment of common diseases in the tropics.
- 6
In travellers who have returned from the tropics and present to the emergency department, common infections not specific to the tropics should not be forgotten as likely causes. A good history and systematic approach may aid in the correct identification of tropical diseases. Expert consultation may be of great benefit and public health notification is essential.
Acknowledgement
The author wishes to thank Professor Bart Currie, Infectious Diseases Physician at Royal Darwin Hospital and the Menzies School of Health Research, for his helpful suggestions.
The author strongly recommends checking all drug doses and regimens carefully. The latest version of the Australian Therapeutic Guidelines (Antibiotic) or other appropriate local guidelines should be consulted.
It is the responsibility of the prescriber to check their patient’s particular circumstances +/- check with their infectious disease specialist and/or local protocols.
Introduction
Tropical diseases cause an enormous burden of disease worldwide, and many other diseases that are not specific to the tropics disproportionately affect people in developing countries.
Returned travellers or migrants may present to health practitioners with signs and symptoms of tropical diseases. Due to climate change and increasing population mobility (travel and migration), health practitioners in non-tropical areas will increasingly need to diagnose and treat tropical diseases. A high index of suspicion, a systematic approach and expert consultation contribute to the appropriate investigation and management of these cases.
Significant areas of northern Australia have a tropical climate, including the Top End (around Darwin), Far North Queensland (north of Cairns) and the Kimberley (in Western Australia). Several tropical diseases are endemic there, with others occurring only infrequently. Indigenous Australians are disproportionally affected by both tropical and non-tropical disease.
Diseases common to temperate climates also occur in the tropics, and it is important to recognize that these may have different aetiologies there. Community-acquired pneumonia in tropical Australia, for instance, is most commonly caused by Streptococcus pneumoniae ; but in severe cases, organisms such as Burkholderia pseudomallei and Acinetobacter baumannii should also be covered. Cryptococcus gattii should be considered in meningitis or subacute pneumonia. In undifferentiated sepsis, melioidosis is an important differential diagnosis. Knowledge of protocols based on specific local circumstances is important.
Vigilant public health systems are in place to help prevent the spread of disease from endemic areas into non-endemic areas. Many of the diseases discussed in this chapter are notifiable in both Australia and New Zealand. An appropriate public health response may include case surveillance, contact tracing and vector control.
Parasitic tropical diseases
Malaria
Introduction and epidemiology
Malaria is often considered the most important tropical disease worldwide. Half of the world’s population is at risk, with over 200 million cases annually. An estimated 429,000 deaths occurred in 2015, of which 92% were in sub-Saharan Africa. A substantial number of malaria infections occur in South America, Southeast Asia and the Pacific.
In Australia, malaria was officially considered eradicated only in 1981, and there are ongoing concerns regarding the potential re-establishment of the disease due to the widespread presence of appropriate vectors and geographic proximity to endemic areas (particularly Indonesia and Papua New Guinea). Around 400 to 500 cases are reported in Australia each year in travellers and migrants.
Malaria is caused by the protozoan parasite Plasmodium , of which six species are currently known to infect humans ( Table 9.11.1 ). They have a complex life cycle and are transmitted by Anopheles mosquitoes, which bite from dusk to dawn. Less commonly, malaria can also be transmitted vertically. The parasites enter the blood and spread to the liver, where they replicate and are periodically released back into the bloodstream and then invade red blood cells.
Table 9.11.1
Plasmodium species that cause malaria in humans
| Plasmodium species | Area | Notes |
|---|---|---|
| P. falciparum (±75%) | Africa, South America, Southeast Asia | Responsible for most severe cases and deaths |
| P. malariae (±20%) | Africa, Southeast Asia, Pacific, South America | Quartan malaria |
| P. ovale curtisi P. ovale wallikeri | West Africa, Southeast Asia | Two subspecies of P. ovale have been described |
| P. vivax | United States, South America, Asia, Africa | Relatively benign |
| P. knowlesi | Southeast Asia (Malaysia) | Can cause severe cases; macaques are a reservoir |
The majority of malaria cases are caused by P. falciparum , which is the most severe and lethal form. Groups at particular risk include young children, pregnant women, immunocompromised patients (including those with HIV/AIDS) and travellers (due to a lack of immunity). Conversely, some genetic red blood cell variations—including sickle cell trait, thalassaemia trait, G6PD deficiency and Melanesian ovalocytosis—provide some resistance against malaria.
Prevention
A large number of national and international organizations are involved in malaria prevention. Measures include vector control programmes, indoor residual spraying, insecticide-treated nets and intermittent preventative treatment for pregnant women. Travellers to endemic areas should use appropriate chemoprophylaxis tailored to the locally occurring Plasmodium species and drug resistance patterns and avoid mosquito exposure. Efforts to develop a malaria vaccine are ongoing.
Clinical features
The incubation period is typically 10 days to 4 weeks, but it can be longer. Mild cases of acute malaria are characterized by paroxysmal fevers caused by periodic parasitaemia. Rigors herald 6 to 10 hours of high fever (>40°C), after which a relatively asymptomatic period follows. The rigors recur after approximately 40 hours (‘tertian’ fever) with P. vivax and P. ovale or approximately 64 hours (‘quartan fever’) with P. malariae . In P. falciparum malaria, fevers are less predictable and may be continuous. Additionally, there may be flu-like symptoms, diarrhoea and mild jaundice.
Chronic malaria occurs when low-level parasitaemia persists, causing recurrent attacks and anaemia, hepatosplenomegaly and increased susceptibility to other infections. Secondary complications include massive splenomegaly, malarial nephropathy and Burkitt lymphoma.
Severe malaria is almost exclusively caused by P. falciparum . Important features are summarized in Table 9.11.2 . The World Health Organisation (WHO) has published case definitions for severe malaria. The prognosis is poor, especially in children. Non-falciparum malaria is usually more benign, but death due to splenic rupture can occur.
Table 9.11.2
Features of severe malaria
From Trampuz A, Jereb M, Muzlovic I, Prabhu RM. Clinical review: severe malaria. Critical Care . 2003;7:315–323.
| Feature | Causes | Signs and symptoms |
|---|---|---|
| Cerebral malaria | Microvascular obstruction with parasite-containing red blood cells | Drowsiness, confusion, coma Delirium, transient psychosis Seizures Focal neurological signs (rare) Usually absent meningeal signs |
| Respiratory distress | Direct capillary damage (ARDS) Respiratory compensation of metabolic acidosis Intercurrent chest infection Anaemia |
Increased work of breathing Kussmaul breathing pattern |
| Severe anaemia | Increased RBC clearance (both infected and non-infected RBCs) Hypersplenism and immunological causes Haemolysis Failing bone marrow erythropoiesis |
Pallor Fatigue, prostration Failure to thrive Jaundice Haemoglobinuria (‘blackwater fever’) |
| Acute renal failure | Pre-renal (dehydration, hypovolaemia) Renal (microvascular obstruction, glomerulonephritis) |
Oliguria, anuria |
| Acidosis | Lactic acidosis | Hyperpnoea (respiratory compensation) |
| Hypoglycaemia | Abnormal liver function Hyperinsulinaemia from quinine/quinidine administration |
Anxiety, diaphoresis Drowsiness, coma Hypothermia |
| Disseminated intravascular coagulation (DIC) | Inappropriate coagulation cascade activation | Bleeding complications Relatively rare (<10% of severe malaria) |
ARDS, Acute respiratory distress syndrome; RBC , red blood cell
Diagnosis
Clinical findings are of limited utility in diagnosing malaria ; microscopic examination of thick and thin blood smears remains essential. A thick smear (drop of blood on a slide) is used to detect the presence of parasites and a thin smear (drop of blood spread thin on a slide) may help to identify the Plasmodium species. One negative smear does not exclude malaria; usually three sets are obtained at 12- to 24-hour intervals. Rapid dipstick immunoassay tests exist but can be falsely negative with low or very high levels of parasitaemia. Plasmodium -specific polymerase chain reaction (PCR) tests are sensitive and specific but not widely available in endemic areas. Many other laboratory abnormalities, such as thrombocytopaenia and hyperbilirubinaemia, can be seen in malaria, but these are not specific enough to make the diagnosis. Before the diagnosis of cerebral malaria can be made, bacterial meningitis should be ruled out by lumbar puncture.
Treatment
Early treatment reduces morbidity, mortality and malaria transmission. Emerging resistance to antimalarial drugs (chloroquine and sulfadoxine-pyrimethamine) is a recurring problem worldwide. Artemisinin, a compound derived from wormwood, combined with another agent (artemisinin combination therapy) is the best currently available treatment for P. falciparum malaria. It is given orally for uncomplicated cases and intravenously for severe cases. Various regimens are available to treat other Plasmodium species. For travellers diagnosed with malaria, different drugs should be used for treatment than were taken for prophylaxis. Initial hospitalization with the consultation of an infectious disease specialist is recommended for all cases.
Schistosomiasis (bilharzia)
This parasitic disease affects more than 200 million people worldwide, with more than 90% of infections occurring in Africa. Its global impact is second only to malaria, with an estimated 200,000 deaths per year and significant chronic morbidity in survivors.
Infected freshwater snails release free-swimming larvae (cercariae) into surface waters, which can penetrate the skin of humans who come into contact with the water. Schistosomula then circulate in the blood and replicate in the portal vessels. Subsequently they migrate to blood vessels in other parts of the body and release their eggs, some of which are shed in human faeces and end up back in the surface waters. The eggs hatch in the water and produce miracidia, which enter suitable freshwater snails. After multiplying inside the snail, cercariae are released into the water, awaiting a new human host. The species of Schistosoma responsible for human infections are listed in Table 9.11.3 ; mixed infections also occur.
Table 9.11.3
Schistosoma species that infect humans
| Schistosoma mansoni | Latin America, Africa, Middle East |
| S. haematobium | Africa, Middle East, Turkey, India |
| S. japonicum | East Asia, Pacific |
| S. intercalatum (±1%) | Sub-Saharan Africa |
| S. mekongi (<1%) | Cambodia, Laos (Mekong river basin) |
Acute infections are more likely to cause symptoms among non-residents of endemic areas. A pruritic rash in response to cercariae entering the skin (swimmers’ itch) can occur within a day, usually subsiding within 10 days. Acute toxaemic schistosomiasis (Katayama fever) is an uncommon but often severe seroconversion illness that may occur 1 to 3 months after the primary infection. Symptoms include fever, malaise, urticaria, cough, diarrhoea, hepatosplenomegaly and lymphadenopathy. It may last several weeks.
In chronic infection, the parasites migrate to species-specific areas in the host body, where their eggs induce a localized inflammatory response with fibrosis. This causes a high burden of disease ; common symptoms are listed in Box 9.11.1 .
Box 9.11.1
Symptoms of chronic schistosomiasis
Hepatosplenic schistosomiasis (hepatic periportal fibrosis)
Intestinal schistosomiasis
|
Genitourinary schistosomiasis
|
Neuroschistosomiasis
Pulmonary schistosomiasis
|
Prevention includes improving sewage management and using personal protection, such as rubber boots. Freshwater exposure should be avoided where possible. Vaccine development has proved challenging.
The diagnosis is made by a history of freshwater exposure and the demonstration of eggs in the urine or faeces. During Katayama fever, no eggs may be seen. Serological tests are available. Abdominal x-rays may show bladder calcification in chronic genitourinary schistosomiasis.
Praziquantel (40 to 60 mg/kg in two divided doses) is an effective treatment but, due to the high rate of re-infection, it may be difficult to achieve a cure in endemic areas. During Katayama fever, prednisone may be given to suppress the acute reaction and a repeat dose of praziquantel is recommended after 1 to 2 months. Community treatment programmes exist in endemic areas.
Leishmaniasis
Various species of Leishmania protozoa occur in South America, Africa, the Middle East and India as well as in southern Europe. They are transmitted by sandflies from human and canine reservoirs. Preventative measures include diethyltoluamide (DEET)-containing insect repellents, covering exposed skin and insecticide spraying inside houses. Sandflies are so small that they will pass through the mazes of bed nets that have not been treated with insecticide.
Leishmania infections can have cutaneous or systemic manifestations depending on parasite species and host factors, and they can remain asymptomatic. HIV co-infection predisposes to severe or recurrent disease. The incubation period is usually 1 to 2 weeks to 6 months, but there can be a latent period of up to 3 years.
Cutaneous leishmaniasis manifests with skin ulcers, which are usually painless unless a secondary bacterial infection occurs. Most lesions heal spontaneously over a few months, leaving a scar. A mucocutaneous form of the disease causes destruction of the mucous membranes of the nose, mouth, throat and surrounding tissues and can occasionally be fatal.
Visceral leishmaniasis (also known as kala-azar) manifests as fever with rigors, malaise, anorexia, lymphadenopathy and non-tender hepatosplenomegaly. Malnutrition and anaemia occur as the disease becomes chronic. The mortality is very high within 2 years if the disease remains untreated, although milder chronic forms also occur.
The diagnosis can be confirmed by microscopy, culture or PCR. Treatment of leishmaniasis varies by clinical manifestation and geographic region; pentavalent antimony-containing preparations are often the most effective drugs.
Post–kala-azar dermal leishmaniasis (PKDL) can occur several months to years after recovery from visceral leishmaniasis and consists of maculopapular lesions that spread from around the mouth. It typically disappears within a year without treatment but may require several months of treatment in some regions. PKDL patients can be long-term reservoirs of infection.
Trypanosomiasis
American trypanosomiasis (Chagas disease)
A major public health concern in Latin and South America, Chagas disease is caused by the flagellate protozoan Trypanosoma cruzi . It is spread to humans and other mammals by the faeces of insects of the Triatominae subfamily (‘kissing bugs’). Additionally, it can be spread vertically or by the administration of blood products. Prevention focuses on vector control, including the improvement of housing conditions and the use of insecticides and mosquito nets. Blood products and organ donors in the Americas are screened for T. cruzi .
The acute phase of the infection may cause no or non-specific flu-like symptoms, but it can be fatal in children. Swelling around the site of inoculation in the face or around the eye (Romaña sign) is well described. The infection becomes asymptomatic within approximately 2 months. In the chronic phase, the parasites invade the myocardium and intestinal smooth muscle. The development of cardiomyopathy leads to congestive heart failure and arrhythmias and is fatal in 30% of patients. Dilation of the oesophagus and colon (10%) and neurological involvement may also occur.
The diagnosis can be made by direct visualization of the parasites in blood smears or by serological testing. Benznidazole and nifurtimox are effective treatments if given soon after the infection occurs. Treatment for chronic infections is difficult and side effects are common. Supportive treatment for cardiac and gastrointestinal complications is important.
African trypanosomiasis (sleeping sickness)
This disease of sub-Saharan Africa is caused by Trypanosoma brucei , which is spread by bites of the tsetse fly. Several major epidemics have occurred in the last century and vector control programmes have been successful in reducing the number of cases reported.
Approximately 95% of cases are caused by Trypanosoma brucei gambiense (West and Central Africa). A chancre may develop at the site of inoculation, followed by an asymptomatic stage which can last months to years. Symptomatic infection then begins with the haemolymphatic stage, characterized by fever, arthralgias and pruritus. Posterior cervical lymphadenopathy (Winterbottom sign) is common. The neurological stage begins when the trypanosomes invade the central nervous system, causing headaches, personality changes, psychosis and focal motor, extrapyramidal and/or cerebellar signs. The final stages of the disease are characterized by daytime somnolence, seizures, coma and death.
A second type of the disease is caused by Trypanosoma brucei rhodesiense (5%), which occurs in southeastern Africa. Its course is more fulminant, with early multiple organ failure and death.
The diagnosis can be made by direct microscopic observation of the trypanosomes. Several serological screening tests (card agglutination trypanosoma test) exist for Gambian trypanosomiasis. The treatment is complex and depends on parasite subtype, regional drug resistance and the stage of the disease.
Filariasis
This variable disease is caused by a number of helminth species (worms) that occur throughout the (sub)tropics and are spread by mosquitoes and black flies. Lymphatic filariasis is the most common form; the worms develop in the lymphatic system and cause lymphoedema. Elephantiasis is the most extreme manifestation of this disease. Subcutaneous filariasis is caused by different species of helminths, producing a rash and arthritis. Onchocerca volvulus inhabits the eyes and is the world’s second cause of blindness (‘river blindness’). The diagnosis can be made with thick and thin blood smears obtained on a species-specific time of the day or by PCR. Treatment is with diethyl-carbamazine or ivermectin and albendazole; sequelae often remain chronic.
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