Infectious Diseases: Listeriosis, Meningitis, Coxsackievirus, Rabies, and More
Listeriosis
Definition
Listeriosis is a severe infection caused by Listeria monocytogenes, affecting neonates, pregnant women, the elderly, and immunocompromised individuals.
Causative Organism
Organism: Listeria monocytogenes
Characteristics: Gram-positive, facultative intracellular bacterium, grows at low temperatures.
Pathogenesis
- Ingested through contaminated food (e.g., unpasteurized dairy).
- Crosses the intestinal barrier, survives inside host cells, and spreads to organs like the brain (causing meningitis) and placenta.
- Evasion of immune response via actin-based motility within cells.
Lab Diagnosis
- Microscopy: Gram-positive bacilli seen in CSF or blood.
- Culture: Grows on blood agar; motility test shows an umbrella shape.
- PCR: Detects Listeria DNA in clinical samples.
Clinical Features
Neonates: Meningitis, sepsis, or granulomatosis infantiseptica.
Pregnant women: Fever, muscle aches, risk of miscarriage or stillbirth.
Elderly/immunocompromised: Meningitis, encephalitis, sepsis.
Treatment
First-line: Ampicillin or Penicillin + Gentamicin.
Alternative: Trimethoprim-sulfamethoxazole for allergies.
Prophylaxis
Avoid unpasteurized dairy, deli meats.
No vaccine; food safety measures are key.
Tubercular Meningitis
Definition
A severe infection of the meninges caused by Mycobacterium tuberculosis, commonly in immunocompromised individuals.
Causative Organism
Organism: Mycobacterium tuberculosis
Characteristics: Acid-fast bacilli, slow-growing, obligate aerobe.
Pathogenesis
- M. tuberculosis spreads from the lungs via bloodstream to the meninges.
- Causes chronic inflammation and granuloma formation, leading to cerebral complications like hydrocephalus and nerve damage.
Lab Diagnosis
- CSF: Low glucose, high protein, elevated WBC (mainly lymphocytes).
- Ziehl-Neelsen stain: Shows acid-fast bacilli.
- Culture: Lowenstein-Jensen medium for slow-growing bacteria.
- PCR: Faster detection.
- Imaging: MRI/CT shows hydrocephalus and meningeal enhancement.
Clinical Features
Fever, headache, vomiting, neck stiffness, altered mental status, cranial nerve palsies, seizures, and signs of increased intracranial pressure.
Treatment
RIPE regimen: Rifampicin, Isoniazid, Pyrazinamide, Ethambutol.
Steroids: Dexamethasone to reduce inflammation.
Prophylaxis
BCG vaccination, early detection and treatment of pulmonary tuberculosis.
Coxsackievirus
Definition
Coxsackievirus is an enterovirus that causes a range of illnesses, from mild conditions like hand, foot, and mouth disease (HFMD) to severe diseases like viral meningitis and myocarditis.
Causative Organism
Organism: Coxsackievirus (part of the enterovirus family)
Characteristics: Non-enveloped, RNA virus, two groups—Group A (more associated with skin and mucosal infections) and Group B (linked to more systemic diseases).
Pathogenesis
Transmission:
Fecal-oral route, respiratory droplets, or direct contact with infected surfaces.
Initial Replication:
Replicates in the gastrointestinal tract and spreads to various tissues.
Target Organs:
Group A: Causes HFMD, herpangina, and occasionally aseptic meningitis.
Group B: Associated with myocarditis, pericarditis, and sometimes diabetes.
Lab Diagnosis
CSF Analysis:
Elevated white blood cells (lymphocytes), normal glucose, and elevated protein in cases of meningitis.
Viral Culture:
Isolation of the virus from throat swabs, stool, or CSF on cell cultures.
PCR:
Detects Coxsackievirus RNA in clinical samples like stool, CSF, or throat swabs.
Serology:
Detection of specific antibodies in the blood to confirm recent infection.
Clinical Features
Group A:
Hand, foot, and mouth disease (fever, rash, oral ulcers), herpangina (fever, sore throat, ulcers).
Group B:
Myocarditis (chest pain, heart failure), pericarditis, aseptic meningitis, diabetes.
Treatment
Supportive care: No specific antiviral treatment; management focuses on symptoms (fever, pain relief).
Severe cases: Intravenous fluids, corticosteroids, or immunosuppressive therapy in myocarditis.
Prophylaxis
Hand hygiene and avoiding close contact with infected individuals. No vaccine.
Post-Exposure Prophylaxis (PEP) Against Rabies
Post-exposure prophylaxis (PEP) against rabies is a series of medical treatments given to individuals who have been potentially exposed to the rabies virus, typically through bites or scratches from an animal that may be infected.
The main components of PEP are:
- Wound cleaning: Immediately clean the wound with soap and water for at least 15 minutes to reduce the risk of infection.
- Rabies Immunoglobulin (RIG): Administered as soon as possible after exposure, RIG provides immediate passive immunity by directly neutralizing the rabies virus at the site of the wound. It is typically given around the wound area and intravenously.
- Rabies Vaccine: A series of rabies vaccinations are given to help the body produce its own antibodies against the virus. The vaccine is usually administered on days 0, 3, 7, 14, and sometimes 28, depending on the exposure and the individual’s vaccination history.
PEP is effective if administered promptly, ideally within 24 hours of exposure, but can still provide protection if administered up to 7 days after exposure. It is important to consult a healthcare provider for specific advice and treatment.
Japanese B Encephalitis
Definition
Japanese B encephalitis (JBE) is a viral infection of the brain caused by the Japanese encephalitis virus (JEV), primarily transmitted by mosquitoes, leading to inflammation of the brain (encephalitis).
Causative Organism
Organism: Japanese encephalitis virus (JEV).
Family: Flaviviridae.
Characteristics: Arbovirus, transmitted by Culex mosquitoes; a flavivirus similar to Dengue and West Nile viruses.
Pathogenesis
Transmission:
Primarily transmitted through mosquito bites, especially by Culex species, which feed on infected animals like pigs or birds.
Initial Replication:
The virus initially replicates in the skin, lymph nodes, and blood.
Neurotropism:
The virus then crosses the blood-brain barrier, infecting the central nervous system, leading to inflammation, neuronal damage, and encephalitis.
Lab Diagnosis
CSF Analysis:
Elevated white blood cells (lymphocytes), normal glucose, elevated protein in cases of encephalitis.
Serology:
Detection of IgM antibodies against JEV in the CSF or serum (primary diagnostic method).
PCR:
Detection of JEV RNA in CSF or serum during the early stages of infection.
Viral Culture:
Virus isolation from CSF, serum, or tissues (though not commonly used due to time constraints).
Clinical Features
Acute onset: Fever, headache, vomiting, and altered mental status.
Neurological symptoms: Seizures, paralysis, coma in severe cases.
Treatment
Supportive care: Management of symptoms such as seizures, fever, and intracranial pressure.
Anticonvulsants for seizure management, mechanical ventilation.
Prophylaxis
Vaccination:
Japanese encephalitis vaccine (inactivated virus vaccine), recommended in endemic areas and for travelers.
Mosquito control: Use of mosquito nets, insect repellents.
Cryptococcal Meningitis
Definition
Cryptococcal meningitis is a fungal infection of the meninges caused by Cryptococcus neoformans, primarily affecting immunocompromised individuals, especially those with HIV/AIDS.
Causative Organism
Organism: Cryptococcus neoformans
Characteristics: Encapsulated, yeast-like fungus, commonly found in bird droppings and soil.
Pathogenesis
Transmission:
Inhalation of spores from contaminated bird droppings or soil.
Initial Replication:
The fungus primarily infects the lungs but can disseminate via the bloodstream.
Neurotropism:
Cryptococcus crosses the blood-brain barrier, causing meningeal inflammation and granuloma formation in the central nervous system.
Lab Diagnosis
CSF Analysis:
Elevated protein, low glucose, and increased white blood cells (mainly lymphocytes).
India Ink Stain:
Reveals encapsulated yeast cells in the CSF.
Cryptococcal Antigen Test:
Detection of cryptococcal antigens in the CSF or serum (highly sensitive).
Culture:
Isolation of Cryptococcus from CSF, blood, or sputum on fungal culture media (e.g., Sabouraud agar).
Clinical Features
Chronic onset: Fever, headache, nausea, vomiting, and altered mental status.
Neurological symptoms: Stiff neck, seizures, and focal neurological deficits in severe cases.
Treatment
Induction therapy: Amphotericin B + Flucytosine.
Maintenance therapy: Fluconazole to prevent relapse.
Prophylaxis
Antifungal treatment for immunocompromised patients at high risk (e.g., HIV/AIDS patients with CD4 <100 cells/μL).
No vaccine available.
Cerebral Malaria
Definition
Cerebral malaria is a severe neurological complication of Plasmodium falciparum malaria, leading to brain dysfunction and potentially fatal outcomes, especially in young children and immunocompromised individuals.
Causative Organism
Organism: Plasmodium falciparum
Characteristics: Protozoan parasite transmitted by Anopheles mosquitoes, responsible for the most severe form of malaria.
Pathogenesis
Transmission:
Infected mosquito bite injects sporozoites into the bloodstream, which travel to the liver and mature.
Red Blood Cell Infection:
Plasmodium infects red blood cells, and mature parasites clog small blood vessels, particularly in the brain.
Cerebral Involvement:
Parasite-induced cytoadherence leads to microvascular obstruction, causing increased intracranial pressure, edema, and ischemic brain damage.
Lab Diagnosis
Blood Smear:
Thin and thick blood films to detect trophozoites and gametocytes of P. falciparum.
Rapid Diagnostic Test (RDT):
Detects malaria antigens in the blood, providing quick diagnosis.
PCR:
Highly sensitive for detecting Plasmodium DNA, confirming species and parasite load.
Clinical Features
Severe malaria: Fever, chills, headache, vomiting, altered mental status, seizures, and coma.
Neurological signs: Respiratory distress, paralysis, and signs of increased intracranial pressure (papilledema, abnormal posturing).
Treatment
First-line: Artemisinin-based combination therapy (ACT).
Severe cases: Intravenous Artesunate or quinine, followed by supportive care for organ dysfunction (e.g., ventilator support, fluids).
Prophylaxis
Preventive measures: Use of insecticide-treated nets, indoor residual spraying, and antimalarial drugs in high-risk areas.
No vaccine widely available, though research is ongoing.
Neurocysticercosis
Definition
Neurocysticercosis is a parasitic infection of the central nervous system caused by the larval stage of Taenia solium (pork tapeworm), leading to cyst formation in the brain.
Causative Organism
Organism: Taenia solium
Characteristics: Tapeworm; its eggs hatch in the intestines, releasing larvae that can invade tissues, including the brain, causing cystic lesions.
Pathogenesis
Transmission:
Ingestion of T. solium eggs from contaminated food or water, often from fecal-oral contamination.
Larvae Migration:
The eggs hatch in the intestines, releasing larvae that migrate through the bloodstream to form cysts in the brain, muscles, and other tissues.
Neuroinvasion:
Cysts in the brain cause inflammation, seizures, and neurological symptoms due to immune response and direct mechanical pressure.
Lab Diagnosis
CT/MRI:
Shows cystic lesions with scolex (larval head) in the brain.
Serology:
Detection of anti-cysticercus antibodies or antigens in the blood or CSF.
CSF Analysis:
Elevated white blood cells (lymphocytes), normal glucose, and elevated protein.
Biopsy:
Rarely, direct biopsy of the cyst may confirm diagnosis.
Clinical Features
Seizures: Most common symptom, ranging from focal to generalized.
Headache, nausea, and vomiting.
Focal neurological deficits (e.g., weakness, visual problems) depending on cyst location.
Treatment
Antiparasitic drugs: Albendazole or praziquantel to kill cysts.
Steroids: For inflammation control.
Anticonvulsants: For seizure management.
Surgical removal: In some cases, for large or symptomatic cysts.
Prophylaxis
Proper hygiene: Handwashing and avoiding consumption of undercooked pork.
De-worming: Regular de-worming programs in endemic areas.
Free-Living Amoebae Infections
Definition
Free-living amoebae (FLA) infections are caused by amoebae found in soil and water, including Naegleria fowleri, Acanthamoeba, and Balamuthia mandrillaris. These infections can lead to severe neurological diseases, including meningoencephalitis and keratitis.
Causative Organisms
Naegleria fowleri: A thermophilic amoeba causing primary amoebic meningoencephalitis (PAM).
Acanthamoeba: Causes granulomatous amoebic encephalitis (GAE) and keratitis.
Balamuthia mandrillaris: Causes GAE, immunocompromised individuals.
Pathogenesis
Transmission:
Naegleria fowleri: Acquired through nasal inhalation of contaminated water, typically from warm freshwater lakes or hot springs.
Acanthamoeba and Balamuthia: Transmitted via direct contact with contaminated water or soil, or through corneal abrasion, leading to eye infections.
Neurotropism:
After entering the body, the amoebae invade the brain or cornea, leading to inflammation, tissue necrosis, and severe damage.
Lab Diagnosis
CSF Analysis:
Naegleria fowleri: CSF analysis may show elevated white blood cells (pleocytosis), elevated protein, and normal glucose.
Microscopy:
CSF, corneal scrapings, or tissues may reveal trophozoites or cysts of the amoeba on wet mount or Giemsa-stained slides.
Culture:
Amoebae can be cultured in non-nutrient agar with E. coli as a food source.
PCR:
Detection of specific DNA for each organism, highly sensitive for confirming species.
Clinical Features
Naegleria fowleri: Fever, headache, nausea, vomiting, seizures.
Acanthamoeba: Keratitis or GAE (headache, fever, focal neurological signs).
Balamuthia mandrillaris: GAE symptoms, skin lesions, fever.
Treatment
Naegleria fowleri: Amphotericin B and rifampin.
Acanthamoeba: Use amphotericin B.
Prophylaxis
Avoid nasal contact with warm, untreated freshwater. General hygiene, immunocompromised individuals.