There are dozens of species of parasitic diseases, but the CSIM2 course requires you to know about the following:
This protozoal infection has an incubation period of between days and years. Transmission is oro-faecal, usually in the form of ingestion of water contaminated with the cyst form of the parasite, which remains semi-dormant until ingestion. Humans are the sole reservoir for this infection, and it is estimated that 10% of the world's population is infected.
Pathogenesis of Amoebiasis
Post-ingestion, the active amoeba (trophozoites) moves to the intestine where it feeds off bacteria and food particles. It remains asymptomatic (in 90% of people) unless it comes into contact with the mucus-covered lining of the intestine. At this point it secretes enzymes, usually designed to break down cell membranes and proteins of bacteria, on to the cells of the gut lining. This leads to the formation of 'flask-shaped ulcers'. This disease process leads to symptoms ranging from diarrhoea to dysentry. Amoeba can also move to other parts of the body, most commonly the liver, causing liver abscesses.
Giardia lamblia, sometimes referred to as 'beaver fever', is a flagellated protozoal infection which usually infects the duodenum and jejunum. It has an incubation period of 7 days - 3 months, and transmits via the oro-faecal route, or via birds and pets. However, the majority of cases result from drinking of water contaminated with giardia cysts.
Pathogenesis of Giardiasis
Trophozoites multiply in the upper bowel via the process of binary fission. The flagellated protozoa disrupt brush-border enzyme activity, stimulating an inflammatory cytokine response, leading to the secretion of fluid and electrolytes and cell damage. Trophozoites encyst as they then pass through the intestine and become infective. Symptoms include loss of appetite, diarrhea, haematuria, loose or watery stool, stomach cramps, projectile vomiting and bloating.
This is a protozoal infection transmitted by females of some species of sandfly. The classic symptoms of leishmaniasis are skin sores, erupting weeks to months after the patient is bitten. Leishmaniasis is also an important clinical cause of splenomegaly, therefore should be considered as a differential diagnosis in areas where the infection is endemic. Other symptoms of the infection that may arise weeks to months following being bitten may include fever, liver damage and anaemia.
Pathogenesis of Leishmaniasis
The female sandfly will inject the infective stage, metacyclic promastigotes, during blood meals. Once these are phagocytosed by macrophages, they transform into amastigotes . They then leave the macrophages and are transmitted around the body to damage various cell types, leading to the symptoms of leishmaniasis. When another female sandfly then bites the human host, the amastigotes are released into the mid-gut of the sandfly, changing into procyclic, then metacyclic promastigotes, migrating to the proboscis of the sandfly, ready to restart the cycle upon another blood meal.
Human African trypanosomiasis, otherwise known as sleeping sickness, is a protozoal infection transmitted by the tsetse fly. The disease is endemic in some areas of sub-saharan Africa . Symptoms usually present in two stages. The first stage (or haemolymphatic stage) consists of fever, headaches, joint pain and pruritus. This is accompanied by the severe swelling of lymph nodes, including Winterbottom's sign, a classical presentation of trypanosomiasis which involves swelling at the back of the neck, in the posterior chain of lymph nodes. The second stage (or neurological stage) begins when the parasite crosses the blood brain barrier, reaching the central nervous system. The primary symptom of this stage is the disruption of the sleep cycle, leading to the name 'sleeping sickness'. This may involve daytime sleeping and nighttime wakefulness. As neurological symptoms progress, the patient may develop a Parkinson's-like tremor, confusion, hemiparesis and paralysis. The patient may also develop psychiatric symptoms, and, without treatment, coma, organ failure and death.
Pathogenesis of Trypanosomiasis
When having a blood meal, the infected tsetse fly injects metacyclic trypomastigotes into skin tissue, which enter the blood stream via the lymphatic system. At this point, they change into trypomastigotes and replicate by binary fission. As with leishmaniasis, the tsetse fly is reinfected once it takes a blood meal from a human host. Infants can also be infected via vertical transmission, as the trypomastigotes can cross the placenta and infect the foetus.
There are a number of types of schistosomiasis.
- Schistosoma mansoni and Schistosoma japonicum cause intestinal schistosomiasis
- Schistosoma intercalatum or 'bilharzia' causes rectal schistosomiasis
- Schistosoma haematobium causes urinary schistosomiasis
Symptoms of infection include abdominal pain, cough, diarrhoea, fever and fatigue. In chronic presentations it can also cause hepatosplenomegaly, bladder cancer (may present with haematuria) and pulmonary hypertension.
Pathogenesis of Schistosomiasis
Snails acts as vectors for the parasite. Parasite eggs are released into the environment from infected individuals, hatching on contact with fresh water to release free-swimming miracidium. Miracidia infect freshwater snails by penetrating the snail's foot. These then develop in the hepatopancreas of the snail, and emerge into the water as cercariae. The cercariae attach onto human skin and degrade it via enzymes, then travelling via the lungs to the liver. At this point they begin to feed on red blood cells, before producing eggs after 6–8 weeks. These eggs pass through the intestinal wall and leave the body via faeces. The eggs themselves do not damage the body: instead it is the immune response that causes the pathology classically associated with schistosomiasis.
Toxoplasmosis is caused by Toxoplasma gondii, an intracellular protozoan parasite. Its main host is the cat. Found more frequently in immunodeficient patients, it is a frequent infection associated with HIV. The disease can reactivate and cause life-threatening encephalitis or severe neurological damage. Transmission is through one of a number of means:
- Oro-faecal contact with cat faeces
- Organ transplant from carrier
- Handling or consumption of raw meat, i.e. pork
- Vertical transmission, as toxoplasmosis crosses the placenta, causing foetal toxoplasmosis
Pathogenesis of Toxoplasmosis
The Toxoplasma gondii is excreted in cat faeces and ingested in secondary hosts. The active proliferating forms of the organism are called tachyzoites. They can be found in any organ, but occur most commonly in the brain, skeletal muscle and heart muscle. The infection will lie dormant for yeaers and reactivate if a state of immunosuppression is reached.