Pathogenecity and Clinical Features in Sarcomastigophora

Intestinal and extraintestinal

E. histolytica causes two types of amebiasis

4 days to 4 months

Incubation of E. histolytica is highly variable. On average, it ranges —

Cytolysis, Amebapores, Tissue necrosis, mucosal penetration, amebic ulcer, Ameboma

Clinical features of Intestinal Amebiasis

The motility of trophozoites And the tissue lytic activity of the amebic cysteine proteases like histolysis

Cytolysis

The metacystic trophozoites penetrate the columnar epithelial cells in the crypts of Lieberkühn in the colon by:

Are ionophore proteins of ameba capable of insertinf ion channels into liposomes causing lysis of target cell membrane of host cells

What is amebapores?

It is also caused by the lysosomal enzymes of the inflammatory cells surrounding the trophozoites

What is tissue necrosis in intestinal amebiasis?

The ameba produces discrete ulcers with pinhead center and raised edges

What is mucosal penetration in intestinal amebiasis?

The typical lesion seen in Intestinal amebiasis. The ulcere are multiple and are confined to the colon, being most numerous in the cecum and next in the sigmoidorectal region

What is amebic ulcer in intestinal amebiasis?

Large necrotic lesions with ragged and undermined edges and are covered with brownish slough

Multiple ulcers in amebiasis may coalesce to form large — base is formed by muscular coat.

Submucosal layer, but amebae spread laterally in the submucosa causing extensive undermining and patchy mucosal loss

The ulcers in amebiasis generally do not extend deeper than —. Blood vessel erosion may cause hemorrhage

the deep ulcers form scars which may lead to strictures,

The superficial lesions generally heal without scarring, but — partial obstruction and thickening of the gut wall.

a granulomatous pseudotumoral growth may develop on the intestinal wall by rapid invasion from a chronic ulcer. This amebic granuloma or ameboma may be mistaken for are malignant tumor.

What is ameboma in amebiasis?

cecum and rectosigmoid junction

Amebomas are most frequent at??

rectal tenesmus, high fever, abdominal discomfort, anorexia, and nausea (RHAAN)

Systemic manifestations of ameboma are:

enlarged tender liver without detectable impairment of liver function or fever

Extraintestinal Amebiasis

1. Hepatic amebiasis

• The most common extraintestinal complication of amebiasis.

• The history of amebic dysentery is absent in more than 50% of cases. Several patients with amebic colitis develop an ??

repeated invasion by amebae from an active colonic infection or to toxic substances from the colon reaching the liver.

Extraintestinal Amebiasis

1. Hepatic amebiasis

• This acute hepatic involvement (amebic hepatitis) may be due to —

the upper right lobe of the liver. ; painful hepatomegaly.

Extraintestinal Amebiasis

Amebic liver abscess

• Liver abscess may be multiple or more often

  solitary, usually located in —. Cardinal signs of amebic liver abscess is —

Fever, Anorexia, nausea, weight loss and fatigue

Extraintestinal Amebiasis

Amebic liver abscess

— is present in most cases. — may also be present.

leukocytosis; and increased serum transaminases

Extraintestinal Amebiasis

Amebic liver abscess

About third-fourth cases of amebic liver abscess have —. Jaundice develops only when lesions are multiple or when they press on the biliary tract.

lesions are multiple or when they press on the biliary tract.

Extraintestinal Amebiasis

Amebic liver abscess

Jaundice develops only when —

adjacent tissues through the diaphragm into the lung or pleural cavity, pericardium, peritoneal cavity, stomach, intestine, or inferior vena cava or externally through abdominal wall and skin.(DLPPPSIIA)

Extraintestinal Amebiasis

Amebic liver abscess

Untreated abscesses tend to rupture into the —

the lower part of the right lung is the usual area affected.

Extraintestinal Amebiasis

Pulmonary amebiasis

Very rarely, primary amebiasis of the lung may occur by direct hematogenous spread from the colon bypassing the liver, but it most often follow extension of hepatic abscess through the diaphragm and therefore, —

hematogenous spread and through lymphatics. Abscesses in kidney, brain, spleen and adrenals have been noticed.

Extraintestinal Amebiasis

Metastatic amebiasis

Involvement of distant organs is by — . — have been noticed.

severe destruction of brain tissue and is fatal.

Extraintestinal Amebiasis

Metastatic amebiasis

Spread to brain leads to —

anus, colostomy site, or discharging sinuses from amebic abscesses.

Extraintestinal Amebiasis

Cutaneous amebiasis

It occurs by direct extension around —.

Extensive gangrenous destruction of the skin occurs. The lesion may be mistaken for condyloma or epithelioma.

Extensive gangrenous destruction of the skin occurs.

Extraintestinal Amebiasis

Cutaneous amebiasis

—. The lesion may be mistaken for condyloma or epithelioma.

ameboflagellate Naegleria Fowleri (the brain-eating Amoeba).

Primary Amebic Meningoencephalitis (PAM) - It is caused by -

the inhalation of dried cysts. It is caused by Acanthamoeba.

Granulomatous Amebic Encephalitis (GAE) - Develops from —.

the entry of the amebic cyst through abrasions on the Cornea

Chronic Amebic Keratitis (CAK) - Develops from —. It is caused by Acanthamoeba.

nasal mucosa and pass through the olfactory nerve branches in the cribriform plate into the meninges, and brain to

Naegleria fowleri

The amebae invade the — initiate an acute purulent meningitis and encephalitis, called as primary amebic meningoencephalitis (PAM).

2 days to 2 weeks ; the patient experiences anosmia.

Naegleria fowleri

The incubation period varies from —.

In the incubation period, —

fever, headache, vomiting, stiff neck, ataxia, seizure and coma.

Naegleria fowleri

The disease advances rapidly, causing —.

The disease almost always ends fatally within a week (average 5 days).

immunodeficiency, diabetes, malignancies, malnutrition, systemic lupus erythematosus (SLE), or alcoholism.

Acanthamoeba

Infection usually occurs in patients with —

Hematogenously

How does Acanthamoeba spread into central nervous system?

Subsequent invasion of the connective tissue and induction of proinflammatory

Acanthamoeba

— responses lead to neuronal damage that can be fatal within days.

severe edema and hemorrhagic necrosis.

Acanthamoeba

A postmortem biopsy reveals —

Keratitis and encephalitis

Acanthamoeba presents chiefly as two chronic conditions:

An infection of the eye that typically occurs in healthy persons and develops from the entry of the amebic cyst through abrasions on the cornea.

Chronic Acanthamoeba/Amebic Keratitis -

• Majority of such cases have been associated with the use of contact lenses.

permanent visual impairment or blindness.

Chronic Acanthamoeba/Amebic Keratitis -

Keratitis and uveitis can result in —

It is a serious infection of the brain and spinal cord that typically occurs in persons with a compromised immune system.

Granulomatous Amebic Encephalitis —

Granulomatous amebic encephalitis is believed to follow inhalation of the dried cysts.

long and the evolution of the illness is slow

Granulomatous Amebic Encephalitis

The incubation period is —

a widespread infection can affect skin lungs, sinuses, and other organs independently or in combination

Granulomatous amebic encephalitis

Disseminated infection - In immunocompromised states like acquired immunodeficiency syndrome (AIDS), a —

Mucus Diarrhea, Fat malabsorption (Steatorrhea),Dull epigastric pain, Belching, Occasionally, Giardia may colonize the gallbladder, causing biliary colic and jaundice. May cause abnormalities of villous architecture. Increased lymphatic infiltration of lamina propria. Loss of brush border epithelium of intestine.

Giardia lamblia

G. lamblia is typically seen within the crypts of duodenal and jejunal mucosa. Often they are asymptomatic, but in some cases may lead to:

Vitamin A, Vitamin B12, Folic acid, Protein, Xylose, Disaccharides

Giardia lamblia

Children may develop chronic diarrhea, weight loss, sprue-like syndrome, and malabsorption of fat:

failure to develop immunoglobulin A (IgA) against specific Giardia antigen.

Giardia lamblia

Chronic giardiasis may be due to —

squamous epithelium and not columnar epithelium.

Trichomonas vaginalis

T. vaginalis particularly infects —

cysteine proteases, adhesins, lactic acid and acetic acid, which disrupt the glycogen levels and lower the pH of the vaginal fluid

Trichomonas vaginalis

T. vaginalis particularly infects squamous epithelium and not columnar epithelium. It secretes —

petechial hemorrhage and mucosal capillary dilation (strawberry mucosa), metaplastic changes and desquamation of the vaginal epithelium.

Trichomonas vaginalis

Parasite causes —

Intracellular edema and so called chicken-like epithelium

Trichomonas vaginalis

—, is the characteristic feature of trichomoniasis.

urethritis, epididymitis and prostatitis.

Trichomonas vaginalis

Infection is often asymptomatic, particularly in males, although some may develop —

severe pruritic vaginitis with an offensive, yellowish green, often frothy discharge, dysuria and dyspareunia

Trichomonas vaginalis

In females, it may produce —. Cervical erosion is common. Endometritis and pyosalpingitis are infrequent complications.

neonatal pneumonia and conjunctivitis have been reported in infants born to infected mothers

Trichomonas vaginalis

Rarely, — have been reported in —.

4 days to 4 weeks

Trichomonas vaginalis

The incubation period of trichomoniasis is—

African trypanosomiasis (West African sleeping sickness).

Trypanosoma brucei gambiense

T. brucei gambiense causes —The illness is chronic and can persist for many years.

which parasite is localized predominantly in the lymph nodes.

Trypanosoma brucei gambiense

Parasitemia - There is an initial period of parasitemia, following —

intermittent fever, chills, rash, anemia, weight loss and headache.

Trypanosoma brucei gambiense

Trypanosomal Chancre - A painless chancre appears on skin at the site of bite by tsetse fly, followed by —

without central nervous system involvement

Trypanosoma brucei gambiense

Systemic Trypanosomiasis - — is referred to as Stage 1 diseass

hepatosplenomegaly and lymphadenopathy, particularly in the posterior cervical region

Trypanosoma brucei gambiense

In this stage(1), there is — (Winterbottom's sign).

in T. brucei rhodesiense infection

Trypanosoma brucei gambiense

Myocarditis - develops frequently in patients with Stage I disease and is especially common in —

anemia, moderate leukocytosis and thrombocytopenia. High levels of immunoglobulins mainly immunoglobulin M (lgM)

Trypanosoma brucei gambiense

Hematological manifestations seen in stage I include —. —are a constant feature.

occurs after several months, the "sleeping sickness" starts

Trypanosoma brucei gambiense

Stage II involves invasion of central nervous system.

With the invasion of central nervous system, which —

headache, mental dullness, apathy and day time sleepiness ; death from asthenia

Trypanosoma brucei gambiense

Stage II involves invasion of central nervous system.

This is marked by increasing —. The patient falls into profound coma followed by —

lymphocytes, plasma cells and morula cells, which are atypical plasma cells containing mulberry-shaped masses of lgA.

Trypanosoma brucei gambiense

Stage II involves invasion of central nervous system.

Chronic Meningoencephalitis - Histopathology shows the meninges are heavily infiltrated with —

infiltration of the brain and spinal cord, neuronal degeneration and microglial proliferation.

Trypanosoma brucei gambiense

Stage II involves invasion of central nervous system.

Brain vessels show perivascular cuffing. This is followed by —

include raised intracranial pressure, pleocytosis and raised total protein concentrations.

Trypanosoma brucei gambiense

Stage II involves invasion of central nervous system.

Abnormalities in cerebrospinal fluid (CSF) —

acute than the Gambian form ; incubation period of 4 weeks.

Trypanosoma brucei rhodisiense

East African trypanosomiasis - is more — and appears after an —.

Edema, myocarditis and weakness are more prominent in East African sickness.

Headache, diffuse muscle and joint pain are present in majority of the patients.

Trypanosoma brucei rhodisiense

Pathological features are similar in both diseases with some variations:

Lymphadenitis; Febrile paroxysms; Mania and delusions

Trypanosoma brucei rhodisiense

• — is less prominent.

• —quantity of parasite in the peripheral blood.

• Central nervous system involvement occurs early.

• — may occur but the marked somnolence, which occurs in T. brucei gambiense infection is lacking.

1 - 2 weeks. The disease manifests in acute and chronic form.

Trypanosoma cruzi

The incubation period of T. cruzi in man is —. The disease manifests in —

Acute phase occurs soon after infection and may last for 1 - 4 months.

Acute Chagas Disease - Acute phase occurs soon —

within a week after invasion of parasite

Tryponosoma cruzi

Acute Chagas Disease

lt is seen often in children under 2 years of age.

First sign appears —

typical subcutaneous lesion occurring at the site of inoculation

Tryponosoma cruzi

Acute Chagas Disease

Chagoma" is the —Inoculation of the parasite in conjunctiva causes unilateral, painless edema of periocular tissues in the eye called as Romana's sign. This is a classical finding of the acute Chagas disease.

unilateral, painless edema of periocular tissues in the eye called as Romana's sign.

Tryponosoma cruzi

Acute Chagas Disease

Chagoma" is the typical subcutaneous lesion occurring at the site of inoculation. Inoculation of the parasite in conjunctiva —. This is a classical finding of the acute Chagas disease.

fever, lymphadenopathy and hepatosplenomegaly

Tryponosoma cruzi

Acute Chagas Disease

In few patients, there may be generalized infection with .

acute myocarditis and meningoencephalitis

Tryponosoma cruzi

Acute Chagas Disease

The patient may die of —

4-8 weeks, acute signs and symptoms resolve spontaneously and patients ; enter the asymptomatic or indeterminate phase of chronic T. cruzi infection

Tryponosoma brucei rhodisiense

Acute Chagas Disease

Usually within —, then —

The chronic form is found in adults and older children and becomes apparent years or even decades after the initial infection.

Tryponosoma cruzi

Chronic Chagas Disease

inflammatory response, cellular destruction and fibrosis of muscles and nerves that control tone of hollow organs like heart, esophagus, colon

Tryponosoma cruzi

Chronic Chagas Disease

ln chronic phase, T. cruzi produces —, etc. Thus, it can lead to cardiac myopathy and megaesophagus and megacolon (dilatation of esophagus and colon).

acute and chronic phase of the disease causing myocardial and neurological damage in the fetus.

Tryponosoma cruzi

Chronic Chagas Disease

Congenital Infection - Congenital transmission is possible in both —

reticuloendotheliosis resulting from the invasion of reticuloendothelial system

Leishmania donovani

Kala-azar is a — by L. donovani.

disseminate the infection to all parts of the body.

Leishmania donovani

The parasitized macrophages —-

multiply enormously in the fixed macrophages to produce a "blockade" of the reticuloendothelial system

Leishmania donovani

In the spleen, liver and bone marrow particularly, the amastigotes ??. This leads to a marked proliferation and destruction of reticuloendothelial tissue in these organs.

grossly enlarged and the capsule is thickened due to perisplenitis.

Leishmania donovani

Spleen

The spleen is the most affected organ. It is —

absence of fibrosis.

Leishmania donovani

Spleen

Spleen is soft and friable and cuts easily due to ??

red or chocolate in color due to the dilated and engorged vascular spaces.

Leishmania donovani

Spleen

The cut section is —

thin and atrophic.

Leishmania donovani

Spleen

The trabeculae are —

greatly increased in numbers and are loaded with LD bodies.

Leishmania donovani

Spleen

Microscopically, the reticulum cells are —. Lymphocytic infiltration is scanty, but plasma cells are numerous.

heavily parasitized, but hepatocytes are not affected.

Leishmania donovani

Liver

The liver is enlarged.

The Kupffer cells and vascular endothelial cells are —,but ??

prothrombin production is commonly decreased

Leishmania donovani

Liver

Liver function is, therefore, not seriously affected, although —

dilated and engorged ; Some degree of fatty degeneration is seen ;

Leishmania donovani

Liver

The sinusoidal capillaries are —. Some — is seen. The cut surface may show a "nutmeg" appearance.

heavily infiltrated with parasitized macrophages ; which may crowd the hematopoietic tissues.

Leishmania donovani

Bone marrow

The bone marrow is —, which may crowd the —

Peripheral lymph nodes and lymphoid tissues of the nasopharynx and intestine

Leishmania donovani

Bone marrow

?? are hypertrophic, although this is not seen in Indian cases.

infiltration of the bone marrow as well as by the increased destruction of erythrocytes due to hypersplenism.

Leishmania donovani

Severe anemia with hemoglobin levels of 5-10 g/dL may occur in kala- azar, as a result of ?? Autoantibodies to red cells may contribute to hemolysis.

autoimmune basis for the pancytopenia observed in kala-azar.

Leishmania donovani

Bone Marrow

Leukopenia with marked neutropenia and thrombocytopenia are frequently seen. Antibodies against white blood cells (WBCs) and platelets suggest an —

Indian Visceral Leishmaniasis and Post-Kala-azar Dermal Leishmaniasis

Leishmania donovani

Ecological Types: The epidemiology and clinical features of VL and the ecology of the parasite are very different in different geographical areas. The different clinical syndromes have, therefore been considered to be distinct entities and the parasite causing them have been given separate species or subspecies status, as listed here:

anthroponotic disease kala-azar and its sequel PKDL

Leishmania donovani

Indian Visceral Leishmaniasis: Caused by L. donovani producing the ??. The disease is not zoonotic; human beings being the only host and reservoir. Vector is the sandfly, P. argentipes.

remittent with twice daily spikes or intermittent or less commonly continuous : Splenomegaly starts early and is progressive and massive.

Leishmania donovani

Indian Visceral Leishmaniasis

The onset is typically insidious. The clinical illness begins with high-grade fever which may be —. Splenomegaly starts early and is —. It is usually soft and non-tender.

common in most endemic areas except Indian subcontinent

Leishmania donovani

Indian Visceral Leishmaniasis

Hepatomegaly is moderate.

Lymphadenopathy is ??? except ??.

dry, rough and darkly pigmented

Leishmania donovani

Indian Visceral Leishmaniasis

Skin becomes — (hence, the name kala- azar).

anemia, emaciation and loss of weight is seen.

Leishmania donovani

Indian Visceral Leishmaniasis

The hair becomes thin and brittle.

Cachexia with marked —