ملخص

MALARIA

Transmission:

1. It is transmitted by the bite of female anopheline mosquitoes .

2. Blood transmission and by injection.
3. trans-placenta

Effects on red blood cells and capillaries

1. haemolysis of infected red cells and adherence of infected red blood cells to capillaries. in a severe or prolonged attack anaemia may be profound. Anaemia is worsened by dyserythropoiesis, splenomegaly and depletion of folate stores
most severe with P. falciparum
P. vivax and P. ovale invade reticulocytes, and P. malariae normoblasts, so that infections remain lighter.
Haemoglobin S heterozygotes (AS) are protected against the lethal complications of malaria.
2. In P. falciparum malaria, red cells containing schizonts adhere to capillary endothelium in brain, kidney, liver, lungs and gut. The vessels become congested and the organs anoxic.

Clinical manifestation of P. vivax and Ovale

In many cases the illness starts with several days of continued fever before the development of classical bouts of fever on alternate days. Gradually the spleen and liver enlarge and may become tender. Anaemia develops slowly. Relapses are frequent in the first 2 years after leaving the malarious area.

Clinical manifestation of Falciparum malaria:

This is the most dangerous of the malarias. The onset is often insidious,and is often mistaken for influenza. The fever has no particular pattern. Jaundice is common due to haemolysis and hepatic dysfunction. The liver and spleen enlarge and become tender. Anaemia develops rapidly. A patient with falciparum malaria, apparently not seriously ill, may develop dangerous complications


Complications of severe F. malaria:
1-Coma (cerebral malaria)
2-Hyperpyrexia
3. Convulsions
4. Hypoglycaemia
5. Severe anaemia
6. Acute pulmonary oedema
7. Acute renal failure
8. Spontaneous bleeding and coagulopathy
9. Metabolic acidosis
10. Shock ('algid malaria')
11. Aspiration pneumonia
12. Hyperparasitaemia

Clinical manifestation of Malaria due to P. malariae:

This is usually associated with mild symptoms and bouts of fever every third day. P. malariae causes glomerulonephritis and the nephrotic syndrome in children.

Diagnosis:

1. Thick and thin blood films
2. Immunochromatographic


Treatment of P. vivax, P. ovale and P. malariae
P. vivax, P. ovale and P. malariae infections should be treated with chloroquine: 600 mg chloroquine followed by 300 mg in 6 hours, then 150 mg 12-hourly for 2 more days

P. falciparum quinine is the drug of choice 600 mg 8-hourly by mouth is given until the patient is clinically better and the blood is free of parasites This regimen should be followed by a single dose of sulfadoxine 1.5 g combined with pyrimethamine 75 mg
In pregnancy a 7-day course of quinine alone should be given.
If sulphonamide sensitivity is suspected, quinine may be followed by doxycycline 100 mg daily for 7 days..

Radical cure of malaria due to P. vivax and P. ovale

course of primaquine (15 mg daily for 14 days)

Prevention

1. Avoiding mosquito bites:
2. Chemoprophylaxis
A.proguanil 1 – 2 tablets daily
B chloroquine (4-aminoquinolones) 2 tablets weekly
Start 1 W before entering and 4 Ws after leaving the endemic area.

AMOEBIASIS

Amoebiasis is caused by Entamoeba histolytica, which is spread between humans by its cyst. E. histolytica can give rise to amoebic dysentery or extraintestinal amoebiasis .


Pathology
Trophozoite invade the mucous membrane of the large bowel, producing lesions that are maximal in the caecum but found as far down as the anal canal. These are flask-shaped ulcers varying greatly in size and surrounded by healthy mucosa. A localised granuloma (amoeboma), presenting as a palpable mass in the rectum, is a rare complication. This responds well to anti-amoebic treatment so should be differentiated from colonic carcinoma.

Intestinal amoebiasis or amoebic dysentery

1-abdominal pains
2-and two or more unformed stools a day
3-Diarrhoea alternating with constipation
4-stools often have an offensive odour
5-tenderness along the line of the colon, especially over the caecum (which may simulate acute appendicitis)
6- Acute bowel symptoms, with very frequent motions and the passage of much blood and mucus, simulating bacillary dysentery or ulcerative colitis .

Diagnosis

Any exudate should be examined at once under the microscope for motile trophozoites
Antibodies can be detectable by immunofluorescence

Treatment and Prevention

Intestinal amoebiasis responds quickly to oral metronidazole, tinidazole ,Diloxanide furoate
Prevention Personal precautions against contracting amoebiasis consist of not eating fresh uncooked vegetables or drinking unboiled water.

AMOEBIC LIVER ABSCESS

This often occurs without a history of recent diarrhoea.
Amoebic trophozoitesmay enter a portal venous system and be carried to the liver where they multiply rapidly and destroy the parenchyma, causing an amoebic abscess.
A large abscess may penetrate the diaphragm and rupture into the lung, from where its contents may be coughed up. Rupture into the pleural cavity
The less common abscess in the left lobe is difficult to diagnose. There is usually neutrophil leucocytosis and a raised diaphragm, with diminished movement on the right side
The abscess is usually found in the right hepatic lobe. Early symptoms may be local discomfort only and malaise; later, a swinging temperature and sweating. An enlarged, tender liver, cough and pain in the right shoulder are characteristic, but symptoms may remain vague and signs minimal . The absence of toxicity in the presence of a high swinging fever is noticeable

Investigations An amoebic abscess of the liver is suspected from the clinical and radiographic appearances and confirmed by ultrasonic scanning
Antibodies are detectable by immunofluorescence in over 95% of patients with hepatic amoebiasis

Management

Early hepatic amoebiasis responds to treatment with or tinidazole
If the abscess is large or threatens to burst, or if the response to chemotherapy is not prompt, aspiration is required and repeated if necessary.
Rupture of an abscess necessitates immediate aspiration or surgical drainage.
Small serous effusions resolve without drainage.

GIARDIASIS

Infection with G. lamblia,. The parasites attach to the duodenal and jejunal mucosa, causing inflammation.
Clinical features
diarrhoea, abdominal pain, weakness, anorexia, nausea and vomiting. On examination there may be abdominal distension and tenderness
diagnosis
Stools should be examined for cysts.
Duodenal or jejunal fluid gives a higher diagnostic yield
On jejunal biopsy fresh mucus examination may show Giardia on the epithelial surface.


Treatment is with a single dose of tinidazole, or metronidazole once daily for 3 days