Infectious Diseases

Question 1

BOVINE

Bacillary Hemoglobinuria
Clostridium hemolyticum (before Clostridium novyi Type D)

Answer 1

Bacillary Hemoglobinuria in Animals - Comprehensive Veterinary Information

Definitions and Terminology:
- Bacillary Hemoglobinuria (Red Water Disease): Acute toxemia caused by Clostridium haemolyticum.

Causative Agents:
- Pathogen: Clostridium haemolyticum (also known as Clostridium novyi Type D).

Physiopathology:
- Transmission: Ingestion of spores, which remain latent in the liver and germinate under anaerobic conditions caused by liver damage (e.g., liver fluke infestation).
- Pathogenesis: Spores germinate in the liver, producing beta toxin (phospholipase C) that causes intravascular hemolysis, leading to hemolytic anemia and hemoglobinuria.

Clinical Findings:
- Symptoms: Sudden onset of severe depression, fever, abdominal pain, dyspnea, severe diarrhea, and hemoglobinuria. Anemia, jaundice, and edema of the sternum may also be present.
- Lesions: Liver infarcts, bloody fluid in body cavities, hemorrhagic intestines, dark friable kidneys, and purplish red urine in the bladder.

Diagnosis:
- Clinical Signs: Port wine-colored urine, severe depression.
- Postmortem: Liver infarcts with diagnostic confirmation via PCR, IFAT, or other laboratory tests.

Treatment:
- Antimicrobials: High-dose penicillin or tetracyclines.
- Supportive Care: Blood transfusions and fluid therapy.

Control:
- Vaccination: With C. haemolyticum bacterin, given once or twice yearly.
- Management: Control of liver fluke infestation and improved pasture drainage.

For more detailed information, visit the Merck Veterinary Manual on Bacillary Hemoglobinuria in Animals.

Question 2

SMALL ANIMALS-Parasites

Roundworms

Answer 2

Comprehensive List of Important Information on Roundworms in Small Animals

1. Causative Agents:
   
   • Toxocara canis, Toxocara cati, Toxascaris leonina.
   • Zoonotic potential: T. canis and T. cati.
2. Transmission:
   
   • Ingestion of infective eggs, transplacental, transmammary (especially in puppies and kittens).
   • Ingestion of paratenic hosts (e.g., rodents).

1. Infection Process:
   
   • Larvae migrate through liver, lungs, somatic tissues.
   • Adult worms reside in the small intestine.

1. Symptoms:
   
   • Often subclinical; in young animals, poor growth, dull coat, pot-bellied appearance.
   • Severe cases: Vomiting, diarrhea, verminous pneumonia.

1. Methods:
   
   • Fecal examination for eggs, fecal antigen tests.
   • Identification of adult worms in vomitus or feces.

1. Medications:
   
   • Fenbendazole, milbemycin, moxidectin, pyrantel, selamectin.
   • Treatment schedules vary: typically two doses 10-14 days apart.
2. Preventive Measures:
   
   • Regular deworming, fecal monitoring, and prompt disposal of feces.
   • Treatment of pregnant/nursing females and young animals.

For more detailed information, refer to the original Merck Veterinary Manual article.

Question 3

SMALL ANIMAL DIGESTIVE PARASITES

Hookworms

Answer 3

Definitions and Terminology:
- Hookworms: Intestinal nematodes, primarily affecting dogs and cats, leading to significant health issues.

Causative Agents:
- Species:
- Ancylostoma caninum (dogs)
- Ancylostoma tubaeforme (cats)
- Ancylostoma braziliense (dogs and cats)
- Ancylostoma ceylanicum (dogs and cats)
- Uncinaria stenocephala (dogs and cats in cooler regions)

Physiopathology:
- Life Cycle: Eggs pass in feces, hatch in soil, and larvae infect hosts through ingestion, skin penetration, or transmammary routes.
- Larval Migration: Skin penetration, blood to lungs, coughed up, swallowed, mature in intestines. Arrested larvae in tissues can reactivate.

Clinical Findings:
- Acute Anemia: Normocytic, normochromic progressing to hypochromic, microcytic in puppies.
- Chronic Infections: Anemia, melena, hypoproteinemia, weakness, diarrhea.
- Lesions: Hemorrhagic enteritis, pneumonia in pups, dermatitis (interdigital spaces).

Diagnosis:
- Fecal Flotation: Detects thin-shelled, oval eggs.
- Antigen Tests: For hookworm detection.
- Postmortem: Examination of intestines for adult worms.

Treatment:
- Anthelmintics:
- Fenbendazole
- Moxidectin
- Pyrantel pamoate
- Milbemycin
- Nitroscanate
- Supportive Care: Blood transfusions, iron supplements, high-protein diet for severe anemia.
- Drug Resistance: Monitor efficacy post-treatment, especially in A. caninum cases.

Control and Prevention:
- Regular Deworming: Based on age and risk factors.
- Sanitation: Dispose of feces promptly, maintain clean environments.
- Preventive Measures: Treat pregnant bitches, routine fecal checks.

Key Points:
- Zoonotic Potential: A. braziliense and A. ceylanicum can infect humans.
- Drug Resistance: Emerging problem, particularly in the southeastern US.

For further detailed reading, visit the Merck Veterinary Manual.

Question 4

Mange in Horses

Answer 4

Definitions and Causative Agents:
- Sarcoptic Mange: Caused by Sarcoptes scabiei equi; intense pruritus, papules, crusts.
- Psoroptic Mange: Caused by Psoroptes ovis and P. cuniculi; lesions, pruritus.
- Chorioptic Mange: Caused by Chorioptes bovis; pruritic dermatitis on distal limbs.
- Demodectic Mange: Caused by Demodex equi and D. caballi; alopecia, scaling.
- Trombiculidiasis: Caused by trombiculid mites; pruritic papules.
- Straw Itch Mite: Opportunistic infestations from organic material.

Symptoms:
- Pruritus, alopecia, crusting, secondary infections.

Diagnosis:
- Skin scrapings, clinical signs, biopsies.

Treatment:
- Medications: Lime sulfur, ivermectin, moxidectin, permethrin.
- Supportive Care: Clipping hair, anti-inflammatory medications for pruritus.

For more details, visit Merck Veterinary Manual - Mange in Horses.

Question 5

Equine - Digestive

**Potomac Horse Fever*

Answer 5

1. Causative Agent:
   
   • Neorickettsia risticii (gram-negative obligate intracellular bacterium).
   • Associated with aquatic insects and freshwater snails.
2. Transmission:
   
   • Ingestion of insects (caddisflies, mayflies) carrying N. risticii.

1. Infection Process:
   
   • Invades enterocytes of the small and large intestine.
   • Causes acute enterocolitis.

1. Symptoms:
   
   • Early: Depression, anorexia, fever (38.9°–41.7°C).
   • Later: Diarrhea, mild colic, dehydration, sepsis.
   • Complications: Laminitis (20%-30% cases), abortion in pregnant mares.

1. Diagnostic Methods:
   
   • PCR assay for N. risticii DNA in blood/feces.
   • Rising paired titers (serology).
   • Cell culture (time-consuming).

1. Medications:
   
   • Oxytetracycline (6.6 mg/kg IV every 12 hours).
   • Supportive care: Fluids, NSAIDs, cryotherapy for laminitis.

1. Vaccination:
   
   • Inactivated whole-cell vaccines (variable efficacy).
2. Management Practices:
   
   • Reduce insect ingestion by turning off barn lights.

For detailed information, refer to the original Merck Veterinary Manual article.

Question 6

Large Animals

Actinomycosis

Answer 6

• Actinomycosis: A chronic bacterial infection caused by gram-positive, anaerobic bacteria Actinomyces.
• Causative Agents:
  
  • Actinomyces bovis: Lumpy jaw in cattle.
  • A. suis (A. denticolens): Pyogranulomatous mastitis in swine.
  • A. hordeovulneris: Localized abscesses and systemic infections in dogs.
  • A. viscosus: Cutaneous abscesses, pneumonia, pyothorax in dogs.

• Cattle: Slow-growing, firm mass attached to the mandible, facial distortion, loose teeth, dyspnea, ulceration, and fistulous tracts.
• Swine: Pyogranulomatous mastitis, subcutaneous granulomatous lesions, lung and organ abscesses.
• Dogs: Localized abscesses, pyogranulomatous pleuritis, peritonitis, and visceral abscesses.

• Methods: Clinical signs, culture (anaerobic conditions), Gram stain, radiology, cytology, and biopsy.

• Ruminants: Intravenous sodium iodide (70 mg/kg of a 10%-20% solution, repeated at 7-10 day intervals), with antimicrobials like penicillin, florfenicol, or oxytetracycline.
• Swine: Rarely successful; surgical removal may be required.
• Dogs: Surgical debridement, penicillin, cephalosporins, sulfonamides, and repeated chest drainage for pyothorax.

• Cattle: Avoid coarse, stemmy feeds or feeds with plant awns to prevent mucosal damage.

For more detailed information, visit the Merck Veterinary Manual - Actinomycosis in Cattle, Swine, and Other Animals.

Question 7

BOVINE DIGESTIVE

Bovine Viral Diarrea*

Answer 7

Definition & Etiology:
- Bovine Viral Diarrhea (BVD): A disease caused by Bovine viral diarrhea virus (BVDV), a Pestivirus in the Flaviviridae family.
- Transmission: Mainly through direct contact with infected animals or contaminated fomites. Vertical transmission can lead to persistently infected (PI) calves.

Pathophysiology:
- BVDV can cause immunosuppression, leading to secondary infections.
- Cerebellar Hypoplasia: In utero infection during mid-gestation can result in cerebellar hypoplasia in calves, characterized by ataxia, tremors, and inability to stand properly.

Clinical Signs:
- Diarrhea, fever, nasal discharge, immunosuppression, and mucosal disease in PI animals.
- Neurological signs in calves with cerebellar hypoplasia include ataxia, intention tremors, and hypermetric gait.

Diagnosis:
- PCR and virus isolation are used to detect BVDV.
- Serology to identify antibodies in the dam or calf.

Prevention:
- Vaccination: Prophylactic vaccination of breeding animals is essential to prevent vertical transmission and cerebellar hypoplasia in calves.

Treatment:
- No specific antiviral treatment; focus on supportive care and prevention of secondary infections.

For more details, refer to the Merck Veterinary Manual.

Question 8

LEPTOSPIRA IN ANIMALS

Answer 8

Definitions and Terminology:
- Leptospirosis: A zoonotic disease caused by pathogenic serovars of Leptospira.

Causative Agents:
- Pathogens: Leptospira interrogans, Leptospira borgpetersenii.

Physiopathology:
- Transmission: Direct or indirect contact with urine from infected animals, contaminated water, or soil.
- Pathogenesis: Bacteria penetrate mucous membranes or broken skin, spread through the bloodstream, and localize in the kidneys, liver, lungs, and other organs.

Clinical Findings:
- Symptoms: Fever, anorexia, vomiting, dehydration, icterus, renal failure, hemolytic anemia, uveitis, abortion, stillbirths.
- Lesions: Interstitial nephritis, hepatitis, pulmonary hemorrhage.

Diagnosis:
- Tests: Microscopic agglutination test (MAT), PCR, culture, ELISA.
- Sample: Blood, urine, tissue samples.

Treatment:
- Antibiotics: Doxycycline, amoxicillin, penicillin.
- Supportive Care: Fluids, blood transfusions.

Prevention:
- Vaccination: Polyvalent inactivated vaccines.
- Hygiene: Avoid exposure to potentially contaminated environments.

For detailed information, visit the Merck Veterinary Manual on Leptospirosis.

Question 9

EQUINE / Hematic - Lymphatic

Equine Granuclocytic Anaplasmosis

Answer 9

• Causative Agent: Anaplasma phagocytophilum.
• Vector: Ixodes ticks (e.g., I. pacificus, I. scapularis).
• Transmission: Tick bites; seasonal occurrence.

• Fever: Up to 107°–108°F.
• Symptoms: Depression, limb edema, ataxia, anorexia, icterus, petechiation.
• Blood Abnormalities: Leukocytopenia, pancytopenia, thrombocytopenia, cytoplasmic inclusion bodies in neutrophils.

• Tests: PCR, serology, blood smear (Giemsa or Wright-Leishman stain).
• Differential Diagnoses: Viral encephalitis, equine infectious anemia, liver disease.

• Antibiotics: Oxytetracycline.
• Supportive Care: Corticosteroids, fluid therapy, pain management.
• Prevention: Tick control; no vaccine available.

For more information, visit the Merck Veterinary Manual.

Question 10

Toxoplasmosis in Animals

Answer 10

• Toxoplasmosis: A zoonotic parasitic disease caused by the protozoan Toxoplasma gondii.
• Intermediate Host: Animals (including humans) that harbor the asexual stages of the parasite.
• Definitive Host: Cats, which harbor the sexual stages of the parasite in their intestines and shed oocysts in their feces.

• Toxoplasma gondii: An obligate intracellular protozoan parasite with a complex life cycle involving both sexual and asexual stages.

1. Definitive Host (Cat):
   
   • Ingests tissue cysts from infected prey or raw meat.
   • Parasite undergoes sexual reproduction in the intestines, producing oocysts shed in feces.
   • Oocysts become infective in the environment within 1-5 days.
2. Intermediate Host (Various Animals and Humans):
   
   • Ingests infective oocysts from contaminated food, water, or soil.
   • Parasite invades host cells, forming tissue cysts primarily in muscles and the central nervous system.
   • Tissue cysts remain dormant but can reactivate if the host’s immune system is compromised.

• Acute Infection:
  
  • Tachyzoites rapidly multiply and spread throughout the body, causing cell lysis and tissue necrosis.
  • Immune response limits the spread, converting tachyzoites into bradyzoites within tissue cysts.
• Chronic Infection:
  
  • Tissue cysts persist for the life of the host, typically without causing disease unless reactivation occurs.
  • Immunosuppression can lead to reactivation and severe disease.

• Cats (Definitive Host):
  
  • Often asymptomatic.
  • Kittens and immunocompromised cats may show fever, lethargy, anorexia, pneumonia, hepatitis, and neurologic signs.
• Dogs and Other Intermediate Hosts:
  
  • General Signs: Fever, lethargy, anorexia, weight loss.
  • Respiratory: Pneumonia, cough, dyspnea.
  • Neurologic: Ataxia, seizures, paralysis, tremors.
  • Ocular: Uveitis, chorioretinitis.
  • Musculoskeletal: Myositis, lameness.
  • Gastrointestinal: Vomiting, diarrhea, abdominal pain.

1. Clinical Examination:
   
   • History and Physical Exam: Assessing clinical signs and potential exposure risk.
2. Laboratory Tests:
   
   • Serology: Detection of antibodies against T. gondii (IgM, IgG).
     
     • IgM: Indicates recent or acute infection.
     • IgG: Indicates chronic or past exposure.
   • PCR: Detection of T. gondii DNA in blood, CSF, or tissue samples.
   • Histopathology: Identification of tachyzoites or tissue cysts in biopsy samples.
3. Imaging:
   
   • Radiography and Ultrasound: To identify organ involvement (e.g., pneumonia, hepatitis).

1. Antiprotozoal Therapy:
   
   • Clindamycin: 10-12 mg/kg orally every 12 hours for 2-4 weeks.
   • Pyrimethamine and Sulfadiazine: Combination therapy to inhibit folic acid synthesis in the parasite.
     
     • Pyrimethamine: 1 mg/kg orally once daily.
     • Sulfadiazine: 30 mg/kg orally every 12 hours.
   • Trimethoprim-Sulfamethoxazole: Alternative treatment.
     
     • Dosage: 15 mg/kg orally every 12 hours.
2. Supportive Care:
   
   • Fluid Therapy: To maintain hydration and support systemic health.
   • Nutritional Support: Ensuring adequate nutrition during recovery.
   • Anti-inflammatory Drugs: To reduce inflammation and manage pain.
3. Preventive Measures:
   
   • Environmental Management: Regular cleaning of litter boxes, preventing hunting, and feeding commercial diets to cats.
   • Hygiene: Proper handling and cooking of meat, washing hands after handling soil or raw meat.

• Dependent on Severity and Timeliness of Treatment: Early diagnosis and appropriate therapy improve outcomes.
• Chronic Infections: May require long-term management, especially in immunocompromised animals.

• Human Infection: Risk from ingesting undercooked meat, contaminated food or water, or handling cat litter.
• Pregnant Women and Immunocompromised Individuals: High risk for severe disease, including congenital infection.

• Toxoplasmosis is caused by the protozoan Toxoplasma gondii, affecting a wide range of animals, with cats as the definitive host.
• Clinical signs vary by species and may include respiratory, neurologic, ocular, musculoskeletal, and gastrointestinal symptoms.
• Diagnosis involves serology, PCR, and histopathology, with imaging used to assess organ involvement.
• Management includes antiprotozoal therapy (clindamycin, pyrimethamine-sulfadiazine) and supportive care.
• Prognosis varies with the severity of the infection and timeliness of treatment.
• Preventive measures focus on environmental management and hygiene to reduce exposure risk.

This summary provides detailed information on toxoplasmosis in animals, covering definitions, causative agents, pathophysiology, clinical changes, diagnosis, management strategies, prognosis, and zoonotic potential, essential for BCSE test preparation.

Question 11

FELINE - Digestive

Feline Panoeukopenia

Answer 11

Feline Panleukopenia (FPV), also known as feline distemper or feline infectious enteritis, is a highly contagious and often fatal viral disease caused by the feline parvovirus. It primarily affects kittens but can infect cats of any age. The virus is incredibly resilient, persisting in the environment for more than a year unless potent disinfectants are used.

• Direct Contact: Cats can contract FPV through direct contact with infected animals, their secretions (saliva, tears, urine, feces), or contaminated environments (fomites).
• In Utero Transmission: In pregnant queens, the virus can cross the placenta, leading to fetal mummification, miscarriage, stillbirth, or cerebellar hypoplasia in kittens.

• Virus Replication: FPV primarily targets rapidly dividing cells, such as those in the bone marrow, lymphoid tissues, and intestinal crypts.
• Leukopenia: Significant destruction of white blood cells (WBCs), leading to immunosuppression.
• Intestinal Damage: Necrosis of intestinal crypts, leading to villous atrophy and severe gastrointestinal symptoms.

• Early Symptoms: High fever, profound depression, anorexia, vomiting (typically developing 1-2 days after fever onset), and sometimes diarrhea.
• Dehydration: Rapid and severe dehydration, often leading to cats sitting by their water bowl without drinking much.
• Neurological Signs: In cases of cerebellar hypoplasia, ataxia and tremors with normal mentation are observed.
• Duration and Mortality: Illness lasts 5-7 days, with high mortality in kittens under 5 months old.

• Clinical Signs: Based on profound depression, leukopenia (total WBC count < 2,000 cells/mcL is associated with a poor prognosis).
• Laboratory Tests: CBC showing leukopenia and neutropenia, followed by rebound neutrophilia during recovery. Immunochromatographic test kits for fecal CPV antigen are used, though they have variable sensitivity.
• Differential Diagnoses: Include salmonellosis, feline leukemia virus (FeLV), and feline immunodeficiency virus (FIV) infections.

• Supportive Care: Aggressive IV fluid therapy with isotonic crystalloid solutions (e.g., lactated Ringer’s solution), electrolyte supplementation, B vitamins, and glucose if hypoglycemia is suspected.
• Antibiotics: Broad-spectrum antibiotics to prevent secondary bacterial infections. Examples include IV ampicillin combined with gentamicin (once rehydration is achieved) or third-generation cephalosporins like ceftiofur.
• Antiemetics: Medications like maropitant and ondansetron to control vomiting and allow early enteral feeding.
• Plasma Transfusion: Fresh-frozen plasma to support oncotic pressure and provide clotting factors and antibodies.
• Nutritional Support: Early enteral feeding with soft, easily digestible food. Parenteral nutrition is reserved for severe cases.
• Anthelmintics: Fenbendazole for treating concurrent intestinal parasitism.

• Vaccination: Core vaccination includes FPV. Kittens should receive multiple doses starting at 6-9 weeks of age, with boosters every 3-4 weeks until 16-20 weeks old. An additional dose at 26-52 weeks is recommended. Adult cats should be revaccinated triennially.
• Hygiene: Regular cleaning and disinfection of the environment to reduce viral load and prevent transmission.
• Isolation: Infected cats should be isolated to prevent the spread of the virus.

For more detailed information, refer to the Merck Veterinary Manual on Feline Panleukopenia【142†source】【143†source】【144†source】.