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Flashcards in NHP Bacterial Diseases Deck (48)
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Describe transmission of Shigella in NHPs.

Endemic infections maintained by asymptomatic carriers.
Infection and disease with antibody production do NOT provide immunity, and animals may be chronically reinfected.


What enteric pathogen is among the most common, and causes disease in marmosets, tamarins, macaques, baboons, apes, and humans. Significant dehydration is a key feature of clinical presentation. Results in a leukocytosis with a left shift.

Shigella spp. Shigella flexneri most frequently, including serotypes 1a, 2a, 3, 4, 5, 6, and 15.
S. sonnei and S. boydii occur less frequently.

(This could also potentially describe Campylobacter)


Describe typical clinical presentation of Shigella in NHPs.

Overt disease in endemic colonies may not manifest without a precipitating stressful event, such as social group disruption or transport.
Clinical signs typically foul-smelling, liquid stool with mucus, blood. Monkeys are weak and mod-severely dehydrated, needing prompt treatment. Severe localized gingivitis, abortion, and air sac infection can also occur.

Marmosets and tamarins do NOT show diarrhea as a primary sign, but are lethargic, depressed, and dehydrated with dried blood around anus.


Describe typical gross lesions with Shigella in NHPs.

Occur primarily in cecum and colon. Colonic mucosa has fibrinopurulent exudate, and intestinal wall is edematous and hemorrhagic with focal ulceration.
May also see small intestine intususseption, rectal prolapse, splenomegaly, and mesenteric lymphadenopathy.

Gross lesions in marmosets and tamarins are confined to cecum and colon.


What are the most frequent fecal bacterial isolates from subclinical and clinically affected NHPs?

Campylobacter jejuni, and C. coli


How does prevalence of Campylobacter infection in macaques change over time?

Increases with time in captivity.


How does Campylobacter usually present clinically?

Watery diarrhea, with mucohemorrhagic possible. WBC may be normal or may have leukocytosis with left shift. Severe electrolyte abnormalities: Na < 132, Cl < 93 mEq/L, with acidosis, and high anion gap.
Many infections are self-limiting.


What is the antibiotic of choice for Campylobacter?
What other treatment is warranted?

Erythromycin historically, but resistance common so should be based on sensitivity if given at all.

Normonatremic fluids such as Lactated Ringers, or normal saline.


What is the significance of isolating E. coli from a NHP fecal culture with diarrhea?

Questionable since its frequently isolated from clinically normal NHPs.

Enteropathogenic E. coli (EPEC) have been identified in rhesus monkeys with SIV.


What are the most frequently reported serovars of Salmonella spp. In NHPs?

S. typhimurium, S. cholerasuis, S. anatum, S. stanley, S. derby, S. oranienburg


What are the typical clinical signs of salmonellosis in NHPs?

Enteric forms can cause watery diarrhea, sometimes with hemorrhage or mucus; often with pyrexia

Extraintestinal signs include neonatal septicemia, abortion, osteomyelitis, pyelonephritis.


What are the gross pathological signs of Salmonella?

Edema, hyperemia, and rare mucosal ulceration in ileum and colon. Enlargement of spleen and mesenteric lymph nodes may occur.


How should Salmonella be treated in NHPs?

Antibiotic therapy should be reserved for those with severe diarrhea or septicemia to reduce chance of carrier state. Zoonotic potential and difficulty in eliminating carriers may necessitate culling carriers.

Other treatment involves supportive care to address fluid and electrolyte loss.


What can cause fulminating enteric and systemic disease in marmosets, owl monkeys, squirrel monkeys, and Old World monkeys?

Yersinia enterocolitica, Y. Pseudotuberculosis


How does yersiniosis typically present in NHPs?

Macaques: diarrhea, vomiting, severe abdominal pain, mild dehydration, blood-stained feces, abortions and stillbirths possible.

Squirrel monkeys: weak, inactive, enlarges cervical lymph nodes

Owl monkey: weakness, depression, diarrhea, abdominal distension, splenomegaly.


What are the typical gross lesions with Yersinia infections in NHPs?

Multifocal hepatic and splenic necrosis or abscesses
Mesenteric lymphadenopathy
Ulcerative colitis

Squirrel monkeys are unique with cervical lymph node enlargement.


How should Yersinia infections be treated?

Treatment is not usually attempted due to fulminating nature if disease.


What clinical pathology signs usually accompany Yersinia infections in macaques? In owl monkeys?

Macaques: leukocytosis, hypo atresia, hypochloremia, prerenal azotemia, hyperfibrinogenemia

Owl monkeys: neutrophilia with left shift


What are the clinical signs of Lawsonia intracellularis in macaques?

Mild or transient diarrhea, abdominal distension, or can be found dead with no clinical signs. Profound anemia (10% Hct).


What is the most devastating respiratory pathogen in NHPs?

Streptococcus pneumoniae


How is Strep. pneumoniae transmitted, and what are predisposing factors?

Transmitted by aerosol via the upper respiratory tract, middle ear, or mouth.
Stress-related factors predispose, such as capture, transport, quarantine, viral infection, waning passive immunity.


What is the typical clinical presentation of Strep. pneumoniae in macaques?

Usually rapidly progressive. Death may occur within hours of onset of clinical signs.
Signs include panophthalmitis, conjunctivitis, lethargy, incoordination, hypothermia, depressed reflexes, ataxia, muscle tremors, head pressing, nuchal rigidity, nystagmus, leukocytosis with left shift.


What is the typical clinical presentation of Strep. pneumoniae in chimpanzees?

Duration can range from 2-14 days. Sign initially URT with coughing, nasal discharge, followed by neurological signs.


What provides a presumptive diagnosis of pneumococcal meningitis?

Free or phagocytized, encapsulated, Gram positive, diplococci in smears of CSF.


What are the typical gross lesions of Strep. pneumoniae infection in macaques?

Engorgement of meningeal vasculature, thickening and opacification of leptomeninges, purulent exudate over cortex and ventricles. Lesions may extend to spinal cord.
In chronic disease, may see asymmetry of cerebral hemispheres and severe malaria of ventral frontal lobes.
Congestion of lungs, pulmonary edema, acute purulent bronchopneumonia, and gray hepatic action of ventral lung lobes.


What characterizes S. pneumoniae infection microscopically?

Fibrinopurulent leptomeningitis extending into cerebral and cerebellar cortices.
(Fig. 13 on p. 736)


What is the general clinical presentation and the range of susceptible NHP species for Klebsiella pneumoniae?

Pneumonia, meningitis, air sacculitis, septicemia, peritonitis, enteritis.
New and Old World monkeys, and apes.


How is Klebsiella typically diagnosed?

Usually post-mortem. Ante-mortem diagnosis is difficult or impossible due to acute course of disease.
New World monkeys in particular may die from septicemia or peritonitis with no clinical signs.


A _____ incidence of Klebsiella infection has been reported for tamarins, and ______ incidence for owl monkeys.

64%, 25-29%


What gross lesions have been reported for callitrichids with Klebsiella infection?

Fibrinous lobar pneumonia, purulent peritonitis, mesenteric lymphadenopathy.


What gross lesions in rhesus macaques have been reported with Klebsiella infection?

Exudative bronchopneumonia, hemopurulent meningitis


How is Klebsiella treated?

Treatment difficult and not usually attempted due to fulminating course and high incidence if drug resistance.

Vaccination with autogenous vaccines in marmosets, owl monkeys, and squirrel monkeys is successful for prevention.


What clinical signs are associated with Bordatella bronchiseptica in marmosets?

Bilateral mucopurulent nasal discharge, dyspnea during handling, pyrexia. Death resulted in some less than 1 year of age


Which NHP species does Pasteurella multocida affect?

Primarily squirrel monkeys and owl monkeys. But, has also been reported on baboons secondary to surgical procedures, chair restraint, and chronic catheterization.


How does Pasteurella multocida present in squirrel monkeys?

Unsteady gait, nystagmus, head tilt, circling.
Meningitis, otitis media, lymphadenitis, and myocarditis on necropsy.


How does Pasteurella multocida present in owl monkeys?

Pneumonia, pleuritis, meningitis


Describe Nocardia spp.

Aerobic actinomycete found in richly fertilized soil as saprophytes on decaying vegetation.
Nocardia asteroides is most common isolate in NHPs.


How is Nocardia infection transmitted?

Contact with skin wounds, inhalation, or ingestion.


How does Nocardia typically present?

Dyspnea, epistaxis, chronic weight loss, abdominal distension and discomfort, chronic intermittent diarrhea, lethargy, depression.

Radiographically, pulmonary lesions cannot be distinguished from tuberculosis.


What are the gross lesions with Nocardia?

Pulmonary lesions include multinodular to diffuse red to gray areas of consolidation, pulmonary hemorrhage and edema, abscesses, and cavitary lesions.
Draining multinodular cutaneous lesions, or subcutaneous nodules are also possible.

Disseminated norcardiosis with multifocal abscesses in the momentum, mesentery, liver, kidney, and stomach, in addition to focal abscesses in the brain, has been reported in macaques.


What are microscopic characteristics of Nocardia infection?

Multifocal to coalescing pyro granuloma containing sulfur granules with large colonies of filament outs bacteria. Multinucleated giant cells are found. At the periphery.


How is Nocardia treated?

No reports of successful treatments.


Epistaxis and sneezing in cynomolgus macaques?

Moraxella catarrhalis
Gram negative diplococcus


Tuberculosis in NHPs is caused by what species?

Mycobacterium tuberculosis, M. bovis, M. africanum
Distribution and character of lesions is identical with all three.


Gross lesions of tuberculosis in macaques?

Caseous nodules in hilar lymph nodes and lung, large cavitary and coalescing lesions in lung, and tubercles extending into thoracic pleura.
Can be secondary spread to spleen, kidney, liver, various lymph nodes.
Less frequently, tuberculous nodules are in cerebrum, spinal column, momentum, uterus, ovary, peripheral lymph nodes, skin, mammary gland, vertebrae.


Typical microscopic lesions of tuberculosis?

Unencapsulated granulomas with necrotic core. Surrounding core are layers of epithelioid macrophages and lesser numbers of neutrophils, with multinucleate Langerhans' giant cells at the periphery.
Mineralization is uncommon.
Acid Fast Bacilli can be demonstrated within lesions intra- and extracellularly.


Describe the sensitivity and limitations of the tuberculin skin test.

Animals with early or advanced disease may give false negative reactions.
False negatives also can occur with:
1. Concomitant infection with measles virus due to immunosuppressive
2. Concomitant treatment with isoniazid

False positives possible with exposure to Freund's complete adjuvant.


Describe the diagnostic utility of thoracic radiographs for tuberculosis.

Can confirm pulmonary disease but cannot distinguish between tuberculosis, norcardiosis, and cryptococcosis.