Malaria Is A Vector Borne Disease Biology Essay

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Usually, people get malaria by being bitten by an infective female anopheles mosquito. Only anopheles mosquito can transmit malaria and they must have been infected through a previous blood meal taken from an infected person. Malaria transmission can be reduced by preventing mosquito bites with mosquito nets and insect repellents, or by mosquito control measures such as spraying insecticides inside houses and draining standing water where mosquito lay their eggs.

Currently, no vaccine is available for malaria, preventive drugs must be taken continuously to reduce the risk of infection. These prophylactic drug treatments are often too expensive for most people living in endemic areas. Malaria infections are treated through the use of antimalarial drugs, such as quinine or artemisinin derivatives. However, parasites have evolved to be resistant to many of these drugs. Therefore, in some areas of the world, only a few drugs remain as effective treatments for malaria.

1.2.2 Epidemiology

Distribution and impact

Figure 1: Countries which have regions where malaria is endemic as of 2003 - colored yellow. (Malaria, US Centers for Disease Control and Prevention).

The vast majority of cases occur in children under 5 years old (Greenwood et al., 2005). Pregnant women are also especially vulnerable. Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and much of Africa; however it is in sub-Saharan Africa where 85-90% of malaria fatalities occur (Layne 2007). Each year, there are approximately 515 million cases of malaria, killing between one and three million people (Snow et al., 2005). Malaria is commonly associated with poverty, but is also a cause of poverty and a major hindrance to economic development.

In a study recently carried out, it was shown that over half of malaria cases were acquired in Africa, this however supports the literature that states that Africa represents a greater risk of acquiring malaria than Asia. Nigeria, however clearly dominated African countries in number of cases. In Asia, Indonesia was the riskiest area. Central and South America posed little risk for travellers. The following results were the findings obtained from the study; 45% of malaria cases were acquired in Africa, 29% in Asia, and 18% in Central America or Caribbean. In Africa, 69% of cases were acquired during stays in western countries. On three continents, Nigeria, India, and Honduras accounted for the greatest number of cases as reported to the CDC (Centers for Disease Control and Prevention, Malaria Surveillance- United States 1995).

In Africa, malaria ranks the third most common infectious disease after pneumococcal carini acute respiratory infection (3.5%) and Tuberculosis (28%). Plasmodium falciparum is the commonest specie in virtually all parts of Africa accounting for up to 98% of the cases in Nigeria and is associated with significant morbidity and mortality. P. falciparum is responsible for virtually all the features of severe malaria. Other species, which include P. malariae, P. ovale, form up to 2% of the cases, P. vivax is not found among indigenous Nigeria. The level of endemicity of malaria in Africa varies from country to country and sometimes from one part to another within the same country. Some factors are responsible for these variations in endemicity and they include; Rainfall pattern, Altitude, and Temperature. High rainfall pattern is associated with high malaria transmission while places with high altitude and low temperatures tend to be associated with lower rates of transmission.

1.2.3 Aetiology

Malaria is caused by protozoan parasites of the genus plasmodium (phylum Apicomplexa). In humans, malaria is caused by plasmodium falciparum, plasmodium malariae, plasmodium ovale, plasmodium vivax and plasmodium knowlesi.

Plasmodium falciparum; It is the most dangerous of these infections as p. falciparum (or malignant) malaria has the highest rates of complications [like cerebral malaria (symptoms of which include impaired consciousness, convulsions, neurological disorder, and coma), advanced immunosuppresssion ] and mortality. In addition, it accounts for 80% of all human malaria infections and 90% of deaths. It does not have a significant exo-erythrocytic stage but has an erythrocytic cycle of 48hours in man.

Plasmodium malariae; It is closely related to p. falciparum and p. vivax which are responsible for most malaria infection. While found worldwide, it is so-called “benign malariaâ€Â and is not nearly as dangerous as that produced by P. falciparum or P. vivax. P. malariae causes fever that reoccur at approximately three-day intervals (a quartan fever), longer than two-day (tertian) intervals of other malaria parasites. It does not have an exo-erythrocytic stage of infection. In some patients, p. malariae can cause serious complications such as nephrotic syndrome (Singh et al., 2004).

Plasmodium ovale; It causes tertian malaria. It is closely related to P. falciparum and P. vivax. It is rare compared to these two parasites and substantially less dangerous than p. falciparum. It has a 72-hour life cycle with a dormant exo-erythrocytic stage.

Plasmodium vivax; It is the most frequent and widely distributed because of recurring (tertian) malaria. Unlike p. falciparum, P. vivax does not cause a severe form of malaria and is hardly fatal. It also has an erythrocytic cycle of 48-hours and a dormant exo-erythrocytic stage that can persist for several years causing relapses.

Plasmodium knowlesi; This is a primate malaria parasite commonly found in Southeast Asia. It causes malaria in long- tailed macaques (macaca fascicularis) but it may also infect humans, either naturally or artificially.

1.2.4 Pathogenesis (Life cycle of malaria parasite)

Plasmodium falciparum has a complicated life-cycle, requiring both a human and a mosquito host, and differentiating multiple times during its transmission/infection process.

Figure 2: Schema of the life cycle of malaria parasite (courtesy Dept. of Health and Human Services, Centre for disease prevention, USA).

The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host. Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.)

After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect red blood cells. The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease.

The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal. The parasites’ multiplication in the mosquito is known as the sporogonic cycle. While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes. The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle.

Content source: Division of Parasitic Diseases National Center for Zoonotic, Vector- Borne, and Enteric Diseases ( ZVED).

1.2.5 Clinical manifestations

Malaria is a febrile illness characterised by fever and related symptoms. However it is very important to remember that malaria is not a simple disease of fever, chills and rigors. In fact, in a malarious area, it can present with such varied and dramatic manifestations that malaria may have to be considered as a differential diagnosis for almost all the clinical problems! Malaria is a great imitator and trickster, particularly in areas where it is endemic.

Clinical manifestations of malaria may greatly vary depending on a number of factors summarized below;

Parasite- related;

Species and Strain; Plasmodium falciparum (malignant) has the highest rates of complications.

Geographic origin; Malaria is presently endemic in Africa, America and South-East Asia.

Host- related;

Age; Children and elderly are more susceptible.

Immune status; Immune- naive individuals have most severe infection.

Pregnancy; Pregnant women are more susceptible to severe infection.

Nutritional Status; Malnourished individuals are more susceptible.

The incubation period for malaria may vary from days to months and even years. However, on average, it is 9-14 days for P. falciparum, 12-17 days to 6-12 months for P. vivax, 16-18 days or more for P. ovale, and 18-40 days or more for P. malariae.

All the clinical features of malaria are caused by the erythrocytic schizogony in the blood. The first symptoms of malaria after the pre-patent period (period between inoculation and symptoms, the time when the sporozoites undergo schizogony in the liver) are called the primary attack. It is usually atypical and may resemble any febrile illness. As the disease gets established, the patient starts getting relapse of symptoms at regular intervals of 48-72 hours. The primary attack may spontaneously abort in some patients and the patient may suffer from relapses of the clinical illness periodically after 8-10 days owing to the persisting blood forms of the parasite. These are called as short term relapses (recrudescences). Some patients will get long term relapses after a gap of 20-60 days or more and these are due to the reactivation of the hypnozoites in the liver in case of vivax and ovale malaria. In falciparum and malariae infections, recrudescences can occur due to persistent infection in the blood.

Manifestations of acute malarial illness

Typical features: It includes three stages viz. Cold stage, Hot stage and Sweating stage. The febrile episode starts with shaking chills, usually at mid-day between 11 a.m. to 12 noon, and this lasts from 15 minutes to 1 hour (the cold stage), followed by high grade fever, even reaching above 1060 F, which lasts 2 to 6 hours (the hot stage). This is followed by profuse sweating and the fever gradually subsides over 2-4 hours. These typical features are seen after the infection gets established for about a week. The febrile paroxysms are usually accompanied by headaches, vomiting, delirium, anxiety and restlessness. These are as a rule transient and disappear with normalization of the temperature.

In vivax malaria, this typical pattern of fever reoccurs once every 48 hours and this is called as Benign Tertian malaria. Similar pattern may be seen in ovale malaria too (Ovale tertian malaria). In falciparum infection (Malignant tertian malaria), this pattern may not be seen often and the paroxysms tend to be more frequent (Sub-tertian). In P. malariae infection, the relapses occur once every 72 hours and it is called Quartan malaria.

Atypical features:

In an endemic area, malaria often presents with atypical manifestations;

Atypical fever: In an endemic area, it is rather unusual to find cases with typical fever pattern. Some patients may not have fever at all and may present with other symptoms listed below. Many present with fever of various patterns - low grade to high grade, with or without chills, intermittent to continuous, or even as cases of prolonged fever.

Headache: Headache may be a presenting feature of malaria, with or without fever. It can be unilateral or bilateral. Sometimes the headache could be so intense that it may mimic intra-cranial infections or intra-cranial space occupying lesions. It may also mimic migraine, sinusitis etc. Presence of projectile vomiting, papilloedema, neck stiffness and focal neurological signs would suggest other possibilities.

Body ache, back ache and joint pains: These symptoms are fairly common in malaria. These can occur even during the prodromal period and at that stage these are generally ignored and diagnosis of malaria is impossible owing to lack of peripheral parasitemia. They are also common accompaniments of the malaria paroxysm. Sometimes, malaria may present only with these symptoms, particularly in cases of recurrent malaria.

Dizziness, vertigo: Some patients may present with dizziness or vertigo, with or without fever. They may also have associated vomiting and/or diarrhoea. Rarely patients may present with swaying and cerebella signs. Drugs like chloroquine, quinine, mefloquine and halofantrine can also cause dizziness, xvertigo, and tinnitus.

Altered behaviour, acute psychosis: Patients may present with altered behaviour, mood changes, hallucinosis or even acute psychosis, with or without fever. Malaria may be detected accidentally in such cases and they improve completely with anti malarial therapy. Altered behaviour may also be due to high grade fever or drugs. Antimalarial drugs like chloroquine, quinine, mefloquine and halofantrine can cause restlessness, hallucinations, confusion, delirium or even frank psychosis.

Altered sensorium: Patients with P. falciparum malaria may present with altered sensorium due to severe infection, hypoglycaemia, electrolyte imbalance due to vomiting or diarrhoea (particularly the elderly), hyperpyrexia, subclinical convulsions etc. Differential diagnosis will include acute encephalitis, meningitis, metabolic encephalopathy etc. As a rule of the thumb, malaria should be considered a possibility in all cases of acute neuropsychiatric syndromes and in cases of proven malaria, other possibilities should be considered in the presence of papilloedema, increased ICT, neck stiffness and focal deficits.

Convulsions, coma: Patients with cerebral malaria present with generalised seizures and deep unarousable coma. Sometimes one single fit can precipitate deep, unarousable coma. These could also be due to hypoglycaemia and all patients presenting with these manifestations should be administered 25-50% dextrose immediately. Drugs like chloroquine, quinine, mefloquine and halofantrine may also trigger convulsions.

Cough: Cough may be a presenting feature of malaria, particularly P. falciparum infection. Patient may have pharyngeal congestion and features of mild bronchitis. Patients who have persistent cough and/or fever even after clearance of parasitemia should be evaluated for secondary bacterial pneumonias/ bronchopneumonia and bronchitis.

Breathlessness: In severe falciparum malaria, patients may present with history of breathlessness, due to either severe anaemia or non-cardiogenic pulmonary oedema. Secondary respiratory tract infections and lactic acidosis are other rarer causes for tachypnoea and/or breathlessness in these patients. Patients with pre-existing cardio-vascular or pulmonary compromise may deteriorate or even die if they suffer from severe malaria.

Chest pain: Acute retrosternal or precordial pain may be presenting feature of malaria. It may radiate to the left or right shoulder tips or arms. This pain may mimic acute myocardial infarction, pleurisy, neuralgia etc. Coupled with breathlessness, sweating and hypotension (algid malaria), the picture will very closely resemble that of acute MI.

Acute abdomen: Patients can present with acute abdominal pain, guarding and rigidity, mimicking bowel perforation, acute appendicitis, acute cholecystitis, ureteric colic etc.

One such patient presented with pain abdomen and vomiting with low grade fever, and on examination had tenderness in the right lower abdomen. He was posted for appendicectomy. Pre operative blood test revealed P. falciparum malaria and he recovered completely with anti malarials!

Weakness: Sometimes patients may present with history of weakness, malaise and prostration. On examination they may have significant pallor, hypotension, dehydration etc. Algid malaria may present like this and the patient may not have fever at all. Chloroquine is also known to cause profound muscular weakness.

Vomiting and diarrhoea: Malaria can present as a case of acute gastroenteritis with profuse vomiting and watery diarrhoea (Choleric form). Vomiting is very common in malaria and is due to high grade fever, the disease itself or even drugs. Vomiting may pose problems in administering antimalarial treatment. These could also be due to drugs like chloroquine and due to secondary bacterial or amoebic colitis.

Jaundice: Patients may present with history of yellowish discoloration of eyes and urine. Mild jaundice is fairly common in malaria and may be seen in 20-40% of the cases. Deeper jaundice with serum bilirubin of more than 3 mg/dL is seen in severe P. falciparum malaria and is associated with anaemia, hyperparasitemia and malarial hepatitis with elevated serum enzymes. Malaria must be considered as a differential diagnosis for all cases of jaundice in a malarious area.

Pallor: Severe anaemia can be a presenting feature of malaria. It is usually normocytic normochromic. It may pose special problems in pregnancy and in children. Pre-existing nutritional anaemia may be aggravated by malaria.

Puffiness of lids: Occasionally patients may present with puffiness of lids, with or without renal dysfunction.

Secondary infections: Malaria produces significant immune suppression and this can result in secondary infections. Common among them are pneumonia, aspiration bronchopneumonia (in the elderly), urinary tract infection, colitis etc. Meningitis and enteric fever have also been reported. In falciparum malaria, severe infection can lead to septicaemic shock (algid malaria).

Hepatosplenomegaly: Patients can present with enlargement of liver and/or spleen, tender or non-tender, with or without fever. Rapid enlargement of spleen or liver in malaria can cause acute pain in the abdomen or chest. Generally, organomegaly is noticed in the second week of malarial illness. However, in cases of relapse or recrudescence, it may be present earlier. Also, in immune compromised patients splenomegaly may be absent. In pregnancy, particularly second half, splenomegaly may be smaller or an enlarged spleen may regress in size due to immune suppression. Although splenomegaly is a cardinal sign of malaria, absence of splenomegaly does not rule out the possibility of malaria.

Combinations of the above: Patients can frequently present with various combinations of the above mentioned symptoms and signs, further confusing the picture.

In all the above listed situations, patients may not have associated fever, thus confusing the picture. In some, fever may follow these symptoms. Therefore, one should not wait for the typical symptoms of malaria to get a blood test done; it is always better to do a smear whenever reasonable doubt exists. (Kakkilaya's Malaria Web Site, Clinical features of malaria).