Tropical diseases

Chapter 65 Tropical diseases

Ramachandran Sivakumar, Michael E. Pelly

Once an exotic and esoteric topic, modern travel and the quest for unusual holidays has the potential to bring tropical diseases to every ICU. This chapter covers some important diseases, which are common in the tropical belt.

MALARIA

EPIDEMIOLOGY AND PATHOGENESIS

It is estimated that four species of Plasmodium (vivax, malariae, ovale and falciparum) cause 300–500 million infections per year. Most of the 1–3 million deaths per year due to malaria are caused by Plasmodium falciparum and the majority of deaths are in children under 5 years in sub-Saharan Africa. Malaria is also widely prevalent in the Indian subcontinent and South-East Asia. It is transmitted from human to human by the bite of infected female Anopheles mosquitoes. After development in the liver, there is invasion of red cells by parasites, which is followed by their multiplication, and rupture of the red cells. The cycle is then repeated in red cells. In vivax and ovale infections, development to dormant forms can occur in the liver, which may lead to relapse.

CLINICAL FEATURES

UNCOMPLICATED MALARIA

Initial symptoms of malaria are non-specific and similar to a viral illness. Classic symptoms of fever, aches, and headache are usually, but not always, present. Other features such as diarrhoea, vomiting, cough, and abdominal pain, may confuse the unwary. Unusual presentations are more common in children and may be missed. Classical rigors or fevers occurring on specific days (tertian or quartan) are usually absent in early falciparum infection. Clinical signs may be unhelpful although hepatosplenomegaly may be present fairly early.

SEVERE MALARIA

Risk factors for severe malaria

• Children under 5 years in endemic regions

• Adults and children in areas of low endemicity

• Non-immune travellers to endemic areas

Definition

The diagnosis of severe malaria requires the presence of one or more of the following with no other confirmed cause occurring in a patient with asexual Plasmodium falciparum parasitaemia:¹

• impaired conscious state

• multiple convulsions

• respiratory distress

• pulmonary oedema

• circulatory collapse

• abnormal bleeding

• haemoglobinuria

• severe anaemia

The incubation period is at least 7 days. The usual range is 9–14 days but this may be longer. Anaemia, jaundice, renal dysfunction, haemostatic abnormalities, thrombocytopenia, pulmonary oedema, shock, hypoglycaemia, and severe metabolic acidosis are common in severe malaria. Several of the above coexist or may develop in rapid succession. Cough, convulsions, and hypoglycaemia are more common in children. Jaundice is common, but hepatic failure is uncommon. The acidosis of malaria is multifactorial and probably very similar to other forms of sepsis involving tissue hypoxia, liver dysfunction, and impaired renal handling of bicarbonate.

The differential diagnosis of malaria includes:

• meningitis, typhoid fever, septicaemia

• severe influenza, dengue and other arboviral infections

• haemorrhagic fevers

• hepatitis, leptospirosis

• rickettsial diseases, e.g. scrub typhus

• relapsing fever (Borrelia recurrentis)

• febrile convulsions in children

Pregnancy increases the risk of development of severe malaria. During pregnancy both maternal and fetal morbidity and mortality are increased.

Poor prognostic indicators include age under 3 years, cerebral malaria, circulatory collapse and organ dysfunction. Laboratory evidence of poor prognosis includes hyperparasitaemia (> 250 000/μl or > 5%), peripheral schizontaemia, severe anaemia (PCV < 15% or Hb < 50 g/l), raisedblood urea > 60 mg/dl and serum creatinine > 265 μmol/l (> 3.0 mg/dl), raised venous lactate (> 5 mmol/l), raised CSF lactate (> 6 mmol/l), low CSF glucose and a very high concentration of TNF-α.

Cerebral malaria

Cerebral malaria may be the most common non-traumatic encephalopathy worldwide. The term is restricted to the syndrome in which altered consciousness due to malaria could not be attributed to convulsions, sedatives, hypoglycaemia or to a non-malarial cause. It is distinguished from the postictal state if unconsciousness persists for more than 30 minutes after a convulsion.

Clinical, histopathological and laboratory studies have suggested two potential mechanisms:

• mechanical hypothesis – cytoadherence of parasitised erythrocytes

• cytotoxic hypothesis – neuronal injury by malarial toxin and excessive cytokine production.

Cerebral malaria has few specific features, but there are differences in clinical presentation between African children and non-immune adults.²

Clinical findings include:

• convulsions

• raised intracranial pressure

• hypoglycaemia

• abnormalities of tone and posture (the commonest being symmetrical pyramidal signs)

• retinopathy – retinal haemorrhages, cotton wool spots, papilloedema, retinal whitening and retinal vessel abnormalities, all of which are more common in children.

DIAGNOSIS

Microscopy of thick and thin films remains the gold standard for both the diagnosis and to follow the efficacy of treatment. In the non-immune patient there is a close association between parasite levels and complications; however, severe complications can occur in patients with low counts.

Rapid diagnostic tests (RDTs) which detect specific antigens (proteins) produced by malaria parasites are useful in diagnosis. Current tests are based on the detection of histidine-rich protein 2 (HRP2) (which is specific for P. falciparum), pan-specific or species-specific parasite lactate dehydrogenase (pLDH), or other pan-specific antigens such as aldolase. Many commercial assays are available. Some tests detect only one species (P. falciparum), while others detect one or more of the other three species. RDTs do not give information about the parasite load and their sensitivity and specificity decrease at low parasitaemia. Hence, it is important to seek microbiological advice regarding the RDTs used locally.

Polymerase chain reaction (PCR) tests based on detecting malarial DNA are more sensitive than microscopy but are expensive and do not give estimates of parasite load.

TREATMENT OF MALARIA ³

WHO has recently issued new guidelines for the treatment of malaria.

FALCIPARUM MALARIA (Table 65.1)

To counter the threat of resistance of P. falciparum to monotherapies, and to improve treatment outcome, combinations of antimalarials are now recommended by WHO for the treatment of falciparum malaria. Antimalarial combination therapy is the simultaneous use of two or more blood schizontocidal drugs with independent modes of action. Artemisin-based combination therapy (ACT) is the recommended treatment for uncomplicated falciparum malaria.

Table 65.1 WHO recommendations for treatment of uncomplicated P. falciparum malaria

Artesunate + amodiaquine

4 mg/kg of artesunate and 10 mg base/kg of amodiaquine given once a day for 3 days

Artesunate + sulfadoxine–pyrimethamine

4 mg/kg of artesunate given once a day for 3 days and a single administration of sulfadoxine–pyrimethamine (25/1.25 mg base/kg body weight) on day 1

Artesunate + mefloquine

4 mg/kg of artesunate given once a day for 3 days and 25 mg base/kg of mefloquine, usually split over 2 or 3 days

Artemether–lumefantrine

Are available as co-formulated tablets containing 20 mg of artemether and 120 mg of lumefantrine. The recommended treatment for persons weighing more than 34 kg is 4 tablets twice a day for 3 days

One of the following ACTs is currently recommended: artesunate + amodiaquine, artesunate + sulfadoxine–pyrimethamine, artesunate + mefloquine, or artemether–lumefantrine. The choice of ACT in a country or region will be based on the level of resistance of the partner medicine in the combination.

Severe falciparum malaria (Table 65.2)

Two classes of drug are currently available for the parenteral treatment of severe malaria: the cinchona alkaloids (quinine and quinidine) and the artemisinin derivatives (artesunate, artemether and artemotil). Recent evidence ^4,⁵ suggests superior efficacy of artesunate over quinine in adults. The dosage of artemisinin derivatives does not need adjustment in vital organ dysfunction.

Table 65.2 WHO recommendations for treatment of severe P. falciparum malaria

2.4 mg/kg i.v. or i.m. given on admission (time = 0), then at 12 hours and 24 hours, then once a day is recommended in low transmission areas or outside malaria endemic areas. If artesunate is not available, quinine i.v. should be used.

For children in high transmission areas, one of the following antimalarial medicines is recommended as there is insufficient evidence to recommend any of these antimalarial medicines over another for severe malaria:

• artesunate 2.4 mg/kg i.v. or i.m. given on admission (time = 0), then at 12 hours and 24 hours, then once a day

• artemether 3.2 mg/kg i.m. given on admission then 1.6 mg/kg body weight per day

• quinine 20 mg salt/kg on admission (i.v. infusion or divided i.m. injection), then 10 mg/kg every 8 hours; infusion rate should not exceed 5 mg salt/kg per hour

Following initial parenteral treatment, once the patient can tolerate it, current practice is to switch to oral therapy and complete a full 7 days of treatment. In non-pregnant adults, doxycycline (3.5 mg/kg per day) is added to quinine, artesunate or artemether and should also be given for 7 days. During pregnancy or in children, clindamycin is used instead of doxycycline.

In patients with features of severe malaria, a mixed infection with falciparum should be assumed even if only a benign species is identified in the film. Occasionally, severe malaria can occur with vivax species. If the clinical suspicion is high, a therapeutic trial of antimalarial treatment is justified, even if the film is negative.

Severe malaria leads to severe septic shock, and the principles of management are the same including resuscitation and provision of supportive treatment. These patients are at risk of acute lung injury but do need adequate fluid resuscitation. Convulsions must be actively treated. Complications should be managed as they present. The threshold for dialysis should be low. Pneumonia and bacterial septicaemia are also common, and should be recognised and treated.

Exchange blood transfusion (EBT) has been used in severe malaria. However, recent WHO guidelines ³ do not recommend EBT, and note the lack of consensus on indications, benefits and dangers involved, or on practical details such as the volume of blood that should be exchanged. Traditional indications for EBT if pathogen-free compatible blood is available are:

• parasitaemia > 30%, even in the absence of clinical complications

• parasitaemia > 10% in the presence of severe disease, especially cerebral malaria, acute renal failure, ARDS, jaundice and severe anaemia and/or poor prognostic factors (e.g. elderly patient, late stage parasites (schizonts) in the peripheral blood)

• parasitaemia > 10% and failure to respond to optimal chemotherapy after 12–24 hours

OTHER FORMS OF MALARIA

Treatment of other forms of malaria is outlined in Table 65.3.

Table 65.3 WHO recommendations for treatment of P. vivax, ovale and malariae malaria

Uncomplicated P. vivax malaria

Chloroquine 25 mg base/kg divided over 3 days, combined with primaquine 0.25 mg base/kg, taken with food once daily for 14 days is the treatment of choice for chloroquine-sensitive infections. In Oceania and Southeast Asia the dose of primaquine should be 0.5 mg/kg.

Amodiaquine (30 mg base/kg divided over 3 days as 10 mg/kg single daily doses) combined with primaquine should be given for chloroquine-resistant vivax malaria.

Complicated P. vivax malaria

Treatment is the same as severe P. falciparum malaria.

P. ovale and malariae malaria

Treatment is the same as uncomplicated vivax malaria but without primaquine for malariae.

PROGNOSIS

Data are largely derived from endemic areas where presentation with convulsions, acidosis or hypoglycaemia is associated with a poorer outcome. Mortality in an artesunate-treated severe falciparum malaria group in one trial ⁵ was still high (15% vs. 22% in quinine-treated patients). In cerebral malaria, mortality is around 20%. The prognosis of cerebral malaria is frequently determined by the management of other complications such as renal failure and acidosis, but neurological sequelae are increasingly recognised.

TUBERCULOSIS

EPIDEMIOLOGY

Tuberculosis continues to be a devastating disease worldwide, with an estimated 8 million new cases and 2.6–2.9 million deaths annually. Medical conditions which predispose to tuberculosis include HIV infection, silicosis, diabetes, chronic renal failure/haemodialysis, malnutrition, solid organ transplant, gastrectomy, jejunoileal bypass, injection and inhalational drug abuse, alcoholism, chronic pulmonary disease and prolonged steroid use. Social factors such as institutional living conditions (nursing homes, homeless shelters, prisons), urban dwelling and poverty are associated with an increased risk of tuberculosis.

PATHOGENESIS

Tuberculosis (TB) is usually caused by Mycobacterium tuberculosis and four others (M. bovis, M. africanum, M. microti and M. canetti) grouped in the Mycobacterium complex. The genus Mycobacterium consists of many different species, all of which appear similar on acid-fast staining.

Inhalation of tubercle bacilli leads to one of four possible outcomes: immediate clearance of the organism, primary or progressive primary disease, chronic or latent infection, and reactivation disease. Latent infection refers to the presence of tuberculous infection (positive tuberculin reaction) without the disease.

The majority of primary TB infections are asymptomatic; clinical pneumonia occurs in 5–10% of adults with a higher incidence in children and those suffering from HIV infection. M. tuberculosis microfoci that have remained dormant after primary infection may undergo reactivation resulting in secondary TB, often referred to as reactivation disease. This is responsible for 90% of TB in patients not infected with HIV.

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Jul 7, 2016 | Posted by admin in CRITICAL CARE | Comments Off

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